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This is just one family's experience with cancer but it provides an idea of what to expect when cancer ambushes your life leaving you shell-shocked; and can possibly dispel some fears of the unknown. Knowledge is power. When cancer entered our lives we were woefully ignorant about it. Nobody talked about their experience with treatment -- only the types of treatment available. So I am sending this message out to cyber space in hopes it reaches the ones that need to hear it. Cancer research has made some incredible discoveries since my loved one was diagnosed so your treatment may be different than what we experienced....hang in there. I will continue to update this post as our journey and experience with cancer continues. Today is January 2, 2016 and I can report that my loved one is working, and making the most of life. All of us value our time together in a way we never did before. In a couple of weeks a full body scan will be performed that will tell us if any visible cancer remains or has returned after several surgeries, radiation and chemo. If the scan comes back clean, my loved one will definitely be more confident going forward. Meanwhile, I try to stay on top of current cancer research in case it rears its ugly head again. At the bottom of this post, I will make notes on cancer research I have encountered. Also, check out my Google+ 'Cancer Experience and Advice' collection for posts on cancer research. Hang in there! You are stronger than you think. Never give up.
Our story began in February 2014 when my loved one bit the inside of the mouth during a dream like many of us do sometime. It did not heal over the course of two months and became more painful. A visit to the dentist and one week of antibiotics did nothing. A visit to the emergency room three months after the initial bite revealed the sore had become a squamous cell cancer tumor creeping up a nerve toward the brain. Lesson learned….if a sore or injury anywhere on the body does not heal in ten days, seek immediate treatment no matter how trivial. It takes just one cell to mutate incorrectly during healing to turn into cancer. Do not stop seeking treatment until the initial injury heals. Being stoic and enduring pain can kill you.
TREATMENT BEGINS – CHEMO AND RADIATION:
The painful oral tumor prevented my loved one from opening the mouth very far making it difficult to examine. No treatment could begin until a dental check up to see if bad teeth needed to be removed prior to radiation and any dental infections had been treated.
Then radiation teeth guards and oral hygiene trays had to be made. The mouth had to be opened to make the molds. It was a very painful and emotional event to watch. Then came the insertion of the chemo port in the neck and surgery to insert a feeding tube. It took approximately a week and a half to complete these preliminary steps before the first chemo treatment.
Chemo and radiation each work differently to destroy cancer. We asked why we can't do one or the other? Why do we need both? The doctor explained doing both is a one-two punch against the cancer -- together they are more effective than done alone.
Our next question was if the tumor should be removed before radiation and chemo. The doctor advised against it because he said radiation and chemo could shrink it or perhaps kill it all together. If it shrunk, less tissue would be destroyed removing it. Since it was surrounding a nerve, it was inoperable unless it shrunk off the nerve.
My loved one is claustrophobic so panic set in when viewing the radiation chamber. A net-like mask made specifically for the patient is used to bolt the patient down on the radiation platform keeping them immobile. You can see through the mask but you are aware you are trapped in it with no one present in the room for the length of the treatment. The radiation is mapped out and programmed so there can be no patient movement. My loved one was bolted down for ten minutes every weekday for seven weeks. A pill was taken to reduce the anxiety but it was still difficult. For the first two weeks, there was no difference in the appearance of the face, but eventually a severe sunburn appearance took hold. It is important that a cream is used anywhere the skin has been radiated to keep it from creating open fissures and peeling off. The radiated skin also tends to wrinkle up like it has been dehydrated unless it is moisturized. Hair around the nape of the neck was lost but has regrown. Wherever the most radiation is received, the hair follicles are destroyed. My loved one lost 90 percent hearing in one ear, one saliva gland, and taste has been altered. Chicken and many other things no longer taste good. Dry mouth will always be a problem and water must be available at all times to keep the mouth and throat wet.
The chemo therapy made my loved one very very sick. A lot of gagging and coughing up phlegm was experienced and sleep could only come one to two hours at a time before the gagging or nausea set in. Lying flat was impossible.
Twice during treatment my loved one experienced a hard ball forming on the face in a place other than the original cancer tumor. Was cancer growing in another nearby spot? Trips to the emergency room revealed an irritated salivary gland and an irritated lymph node -- not a new cancer.
My loved one hated the feeding tube and the liquid given to be used with it caused gas, nausea, and diarrhea. Liquid Ensure via the mouth was the meal of choice. A lot of weight was lost. A comfortable chair and bed near a bathroom is a necessity because there is a lot of fatigue, gagging and throwing up. Too much noise and activity around them causes irritation. However, they should not be left alone to dwell on their condition. They may be irritable, and unpleasant to be around, but still need to vent that irritation. It is best to just listen and let them vent. They need to have some control over their lives since cancer has taken away so much of it. The types of worries expressed can be concern over not being the person they were, that they are no longer useful or are a burden to their loved ones, and fear that they will be abandoned. At the same time that they are irritable, they may also be affectionate realizing that life is short and wanting to express their love while there is time. There may come a time when they do not want to talk about cancer because it is always present and they are weary from the battle. They just want to escape it for a while. If possible and they are up to it, arrange some excursion that distracts them from cancer and don’t mention cancer to them during that time.
My loved one has cancer but the whole family has it too…we are just experiencing it in a different way then the patient. For the first time you entertain life with the possibility that they won’t be in it. It seems impossible and unbearable. Little decisions seem so important because if the wrong treatment is given it could be disastrous, or your loved one could misunderstand what you are saying and be upset. Cancer is always the silent elephant in the room.
Tolerance for the way other family members cope with a loved one’s cancer is also needed. We don’t all react the same way. Just because someone acts strong does not mean they aren’t crying inside.
It’s difficult to sleep because of the flight/fight response you are experiencing in your desire to save your loved one. You may not want to talk about it with others because you have no answers to their questions and retelling the story is the same as reliving it.
After chemo and radiation, scans showed that the oral tumor shrank off the nerve leading to the brain but that cancer remained in the lymph nodes and thyroid in the neck. Extensive oral biopsy showed no cancer cells survived in the oral tumor area after treatment. No surgery was performed to remove anything in the mouth after chemo and radiation. There is a hard spot where the tumor was that may be scar tissue. Jaw mobility without pain was restored although the mouth cannot be opened as wide as before cancer. Some taste on one side of the tongue and some hearing returned. Fatigue remains.
THE MISTAKE WE MADE:
Why, after chemo and radiation, did cancer survive in the neck? It was a mystery until doctors realized my loved one had two different types of cancers at the same time, and they don't both respond to the same treatment. Make sure you are not the rare cancer patient that has more than one type of cancer that goes undetected while being treated for the one type of cancer that is known. Please do not make the mistake we did. We thought my loved one had cancer without realizing that there are many different types of cancers that respond to treatment differently. ==> Treatment for one type of cancer can render another type of cancer 'untreatable'! Because it is rare for a patient to have two types of cancer at once, the doctors treating my loved one did not realize there were two different cancers in play so they recommended a course of treatment for the cancer type they were aware of: Squamous Cell Cancer. The treatment as you know was radiation and chemotherapy followed by surgery.
Later, after radiation and chemotherapy, we found out that Thyroid cancer was also present. A scan revealed that because my loved one was radiated for the squamous cell cancer, the thyroid cancer cells have mutated into untreatable cancer cells. They can spread at will without being detected. A pet scan in some cases can find them but it is not reliable. This is not good news for us because we were relying on removing any cancer that spread and showed up during my loved one's lifetime. My loved one will continue with thyroid cancer treatment including lymph node and thyroid removal, which has been done, and swallowing a radioactive pill and remaining alone for five days. But there is no way to know if the pill will destroy all the thyroid cancer cells still present after surgery since they have mutated and are now resistant to treatment and undetectable.
When you have dental xrays, make sure your thyroid is shielded by the lead vest.
NECK SURGERY AND RESULTS TWO MONTHS AFTER SURGERY:
My loved one’s frontal neck surgery removed the thyroid and 40 lymph nodes of which 12 were cancerous with thyroid cancer -- not squamous cell like the tumor in the mouth. Lymph nodes in the rear of the neck were not touched and because of the prior radiation it cannot be determined if they are cancerous. Even though a daily thyroid medication is taken, my loved one has lost 60 pounds and is very thin. It is hard to tell if that is from the effects of the treatments or if a painful jaw is preventing proper levels of food consumption. For those concerned about scarring from this type of surgery, the scar extends from behind one ear down into the natural neck folds and up to behind the opposite ear in a smile formation.
The neck surgery took nine hours and was closed with staples which were removed painlessly after a week. Three draining tubes were inserted around the neck to drain the fluid buildup at the surgery site. They were removed two days after surgery (after two months, shoulder pain remains which is attributed to those tubes).
Massive doses of calcium are given during the hospital stay to see if the body is absorbing it post surgery. If the body absorbs correctly, the patient can go home to recover. My loved one spent four days in the hospital.
There was swelling in the neck area for a while but then it subsided and the neck looks normal. The neck is stiff and it became painful to hold up without support after surgery. No neck brace can be worn because of the surgical scar in that area. Eventually the neck muscles rebuild and it becomes easier to hold the neck and head up. Physical therapy is recommended because scar tissue can form that prevents neck mobility.
The scar is healing nicely but is still a very thin red smile line which is not that noticeable when looking straight frontal but is noticeable from the side view. The scar is expected to fade over time and does blend in nicely with the natural neck folds. The neck is slightly thinner but not deformed. It is important that a vitamin E cream is used on the scar after it closes and anywhere the skin has been radiated. The radiated skin tends to wrinkle up like it has been dehydrated unless it is moisturized. My loved one needs physical therapy to restore more function and movement to the neck but so far has refused. Without physical therapy and forced movement (even with some pain) scar tissue forms and muscle atrophy will eventually prevent mobility.
THE AFTER EFFECTS OF RADIATION AND CHEMO:
The radiation has caused jaw bone death which was expected around four months after radiation to the neck. My loved one underwent 20 rounds (1.5 hours each) in a hyperbolic chamber to force blood into the dying jaw area to stop the deterioration. During this process, an infection set in in the jaw and antibiotics had to be taken.
It has been weeks since we found out about the jaw bone death, and surgery was performed April 24, 2015 after 20 dives in the hyperbolic chamber. Because radiation to the face and neck tightens and changes the internal structures of the face and neck and makes resuscitation difficult, an air tube prior to surgery sometimes has to be inserted down the nose while the patient is awake prior to complete anesthesia. Luckily, my loved one had enough of an opening and jaw and neck movement that it was not necessary. A roughly 2.5 inch by 5 mm section of jaw bone and three teeth in the left lower rear jaw were removed during outpatient surgery. Blood was taken from my loved one, spun, and the growth factors removed from the blood. The growth factors were injected in the surgery site to induce the growth of blood vessels in the area since much tissue was damaged by the radiation to the side of the face and neck. The surgery took 3 hours from entering the operating room to recovery, and then my loved one went home to recover. Because morphine causes my loved one nightmares, Percocet was prescribed for pain. Even though an extra amount of numbing medication was administered at the end of surgery, pain at a level of 4 (from 1 to 10 with 10 being the worst) was experienced during recovery. Two Percocet, one at a time with a twenty minute wait time, was administered and helped tremendously. There will be a liquid diet the first two days and then a soft diet (scrambled eggs, macaroni and cheese, soups) for the next two weeks.
Ten more hyperbolic chamber dives of 1.5 hours each will be given now that the jaw surgery is complete in an effort to restore blood flow to the jaw.
It has been nearly three weeks since the jaw bone surgery and the ten hyperbolic chamber dives have been completed. The gums are not reattaching to the jaw bone as hoped and another section of dead bone has been found further back from the surgery site. Five more hyperbolic chamber dives are required before a course of treatment will be determined.
May 20, 2015 and the jawbone continues to die. The gums will not heal over the surgery site. No decisions on what to do yet. Wait, wait, wait another week for an answer. It could take a year or more before all the jaw bone that is going to die dies. In the meantime, infection is the immediate enemy. When the exposed dead jaw bone turns yellow, infection can set in and surgery must be performed. Always in the back of our minds is the question of how much jaw bone will be left and will it be disfiguring.
There is hope that the jawbone surgery will be the last surgery needed unless the cancer reappears and is detectable. But if the jaw bone surgery closes incorrectly, infection sets in, or the tissues do not regenerate, additional bone death can occur and more surgery will be required. If more jaw bone needs to be removed, bone will be taken from my loved one’s hip area to replace it. It is all a waiting game from now on.
It’s been a year now since that first cell mutated into cancer and all our lives are forever changed. Cancer is a bitch and it tests your metal in every conceivable way. Bless the oncologists, surgeons, nurses, and peripheral staff that fight this everyday on the front lines.
January 27, 2016. My loved one has had a full body scan that compared this scan with those of the past. It shows NO NEW incidences of cancer, or growth of cancer in previous cancerous areas. Hallelujah! There is a spot on the lung but that may just be a lesion from a previous infection. The next scan will be in six months. The jaw bone continues to deteriorate at the point it was radiated. The dry, brittle area is scraped off from time to time, but the gums stubbornly won't cover it. We are told we will have to wait to see how much jaw bone death will occur. My loved one, while looking well enough, still has lingering effects from chemo and radiation experiencing a tiredness and feeling old nearly a year after treatment. This is normal and may subside with time. There are intermittent sharp pains where the neck incision was made (from ear to ear) and the neck becomes sore and tires easily. My loved one mistakenly continues to refuse physical therapy for the neck and shoulder areas. The incision is no longer pink after a year and has receded nicely into the neck folds, although the cheek is dry and wrinkly from radiation. One doctor has recommended a filler under the skin for that area...not botox. Initially told incorrectly in May 2014 that this was Stage IV cancer, we are so grateful for this outcome to date, and look forward to increasingly better, less invasive, treatment for cancer.
May 9, 2016: Bad news…my loved one’s ultrasound found a 1cm lump on the left side of the neck. The doctors think it's a left over lymph node. My loved ones labs also came back with .2 on thyroid detection... which is low, but according to the doctors indicates thyroid cells are still in the body. My loved one may still have thyroid cancer. The next scan in five months will tell us more.
December 22, 2016: My loved one's two recent biopsies just came back negative for cancer! After radiation, chemo, multiple...too many to count.. hyperbolic chamber dives, dying jawbone, and three surgeries over two years...I'm so incredibly thankful! If you or a loved one has cancer, don't give up. Technology is on your side and winning more and more each day.
RESEARCH NOTES:
5/5/2015: My loved one was diagnosed with squamous cell oral cancer in 2014. Subsequently, after radiation and chemo for the oral cancer, thyroid cancer was found. We knew that there was cancer present in the neck before it was discovered to be thyroid cancer. We thought it was the squamous cell cancer that had spread from the oral tumor.
Why did my loved one have two cancers at the same time? Yes, it could be a coincidence, but one has to wonder if there is something more to it. My loved one had extensive fluoroscopy conducted after removal of uvula for sleep apnea, and swallowed barium during fluoroscopy xray to image the throat several years prior to developing cancer. Online research shows that the FDA was concerned as far back as 2008 about excessive radiation exposure in CT Scans. I am not recommending that anyone refuse a CT Scan or a fluoroscopy necessary for medical treatment, but there does seem to be evidence that cells subject to radiation can become damaged while remaining viable. With their mutated DNA, do they spawn cancer? After reading the articles below, it seems that many people develop leukemia (a blood cancer) years after receiving radiation. Unless I misunderstood the article, it seems a study done in 2008 in San Francisco indicated that not all medical x-rays had consistent levels of radiation, and many times the level of radiation was excessive. It was of enough concern, that the FDA posted a cancer risk notification on it's website.
These are the links I am referring to:
http://www.fda.gov/Radiation-EmittingProducts/RadiationEmittingProductsandPro cedures/MedicalImaging/MedicalX-Rays/ucm115354.htm
http://onlinelibrary.wiley.com/doi/10.3322/caac.21132/pdf
http://www.cancer.gov/cancertopics/causes/radiation/InterventionalFluor.pdf
4/15/2015: HOW IT WORKS: CANCER-FIGHTING IMMUNOTHERAPY
In the war against cancer, doctors have discovered a powerful new tool: the immune system. The FDA recently fast-tracked approval of three new immunotherapy drugs, called PD-1 inhibitors, designed to help white blood cells hunt down and eradicate hard-to-fight tumors--indefinitely. “Chemotherapy almost always stops working,” says Jonathan Cheng, executive director of oncology clinical development at Merck. “The promise of immune therapy is that you’re training the immune system to attack something foreign, so you’re able to maintain that activity for a very long time--hopefully for the rest of a patient’s life.”
Link: http://www.sciencehook.com/hook.php?entryID=360
4/15/2015: Cancer Research on the Evolution of Cancer Cells
Why does cancer go into remission after treatment, and then come roaring back? Cancer starts with one cell mutating in an abnormal way. Scientists mapping the evolution of cancer cells think there is evidence that cancer continues to mutate in stages and those stages do not respond to the same therapy. There may be cancer cells in a tumor in various stages of mutation so therapy will be effective for some parts of the tumor but not others. The tumor is like a family with many children (cells) at various ages that respond differently, e.g. you wouldn’t treat an infant the same as a five year old. Even though the tumor shrinks after treatment, some cancer cells within the tumor will be in a stage that makes them immune to that treatment. It is important that a tumor be analyzed to determine the stage that the majority of its cells are in to determine the most effective treatment. Through the 'evolutionary/family tree' line of research, scientists are hoping to change our ‘Cancer’ game from one of defense to offense. Read about it at: http://www.alwaysresearching.com/2015/04/15/from-snapshot-to-family-tree-writing-the-evolutionary-rule-book-of-cancer/?utm_source=dlvr.it&utm_medium=gplus
4/21/15 Pancreatic Cancer Research: A new research study has shown that pancreatic cancer cells can be coaxed to revert back toward normal cells by introducing a protein called E47. E47 binds to specific DNA sequences and controls genes involved in growth and differentiation. The research provides hope for a new treatment approach for the more than 40,000 people who die from the disease each year in the United States.
“For the first time, we have shown that overexpression of a single gene can reduce the tumor-promoting potential of pancreatic adenocarcinoma cells and reprogram them toward their original cell type. Thus, pancreatic cancer cells retain a genetic memory which we hope to exploit,” said Pamela Itkin-Ansari, Ph.D., adjunct professor in the Development, Aging, and Regeneration Program at Sanford-Burnham and lead author of the study published today in the journal Pancreas. E47 turns the clock back The study, a collaborative effort between Sanford-Burnham, UC San Diego, where Itkin-Ansari holds a joint appointment, and Purdue University, generated human pancreatic ductal adenocarcinoma cell lines to make higher-than-normal levels of E47. The increased amount of E47 caused cells to stall in the G0/G1 growth phase, and differentiate back toward an acinar cell phenotype. - See more at: http://beaker.sanfordburnham.org/2015/04/pancreatic-cancer-breakthrough-scientists-turn-cancer-cells-into-normal-cells/#sthash.oPYWrOHW.dpuf
April 27, 2015 Colon Rectal Cancer:
Author: Chris Jones-Cardiff
Cardiff University Original Study
Posted by Chris Jones-Cardiff on April 27, 2015
You are free to share this article under the Attribution 4.0 International license.
A new study is the first to show that common inherited genetic variants influence life expectancy in patients with colorectal cancer (CRC).
A team from Cardiff University’s School of Medicine analyzed over 7,600 patients with CRC from 14 different centers across the UK and the US. They found that a genetic variant in the gene CDH1 (encoding E-cadherin) was strongly linked to survival.
Having combined data of both inherited genetic variations and variations found within the cancers, the scientists believe that the resulting information will play a crucial role in managing patient survival.
“Our findings show that patients carrying a specific genetic variant, which is found in about 8 percent of patients, have worse survival, with a decrease in life expectancy of around four months in the advanced disease setting,” says study leader Professor Jeremy Cheadle.
“This work shows the potential use of genetic variants to help provide clinically useful information to patients suffering from colon cancer,” says Lee Campbell, science projects and research communications manager from Cancer Research Wales, which part-funded the study.
“Not only does this important piece of research allow clinicians to make more informed treatment decisions for individuals in future, but also has the capability to enhance existing screening or post-operative surveillance programs for this disease.”
“This represents a critical first step to improving colorectal cancer patient outcomes through a greater understanding of the influencing genetic factors,” adds Ian Lewis, director of research and policy at Tenovus Cancer Care.
The Bobby Moore Fund from Cancer Research UK, Tenovus Cancer Care, the Kidani Trust, Cancer Research Wales, and the National Institute for Social Care and Health Research Cancer Genetics Biomedical Research Unit (2011-2015) supported the work.
The findings are available in Clinical Cancer Research.
Source: Cardiff University
http://www.alwaysresearching.com/2015/04/27/gene-variant-linked-to-colon-cancer-survival/?utm_source=dlvr.it&utm_medium=gplus
Original article source: http://www.futurity.org/gene-bowel-colorectal-cancer-907542/
Clinical findings: http://clincancerres.aacrjournals.org/content/early/2015/04/14/1078-0432.CCR-14-3136.abstract
Our story began in February 2014 when my loved one bit the inside of the mouth during a dream like many of us do sometime. It did not heal over the course of two months and became more painful. A visit to the dentist and one week of antibiotics did nothing. A visit to the emergency room three months after the initial bite revealed the sore had become a squamous cell cancer tumor creeping up a nerve toward the brain. Lesson learned….if a sore or injury anywhere on the body does not heal in ten days, seek immediate treatment no matter how trivial. It takes just one cell to mutate incorrectly during healing to turn into cancer. Do not stop seeking treatment until the initial injury heals. Being stoic and enduring pain can kill you.
TREATMENT BEGINS – CHEMO AND RADIATION:
The painful oral tumor prevented my loved one from opening the mouth very far making it difficult to examine. No treatment could begin until a dental check up to see if bad teeth needed to be removed prior to radiation and any dental infections had been treated.
Then radiation teeth guards and oral hygiene trays had to be made. The mouth had to be opened to make the molds. It was a very painful and emotional event to watch. Then came the insertion of the chemo port in the neck and surgery to insert a feeding tube. It took approximately a week and a half to complete these preliminary steps before the first chemo treatment.
Chemo and radiation each work differently to destroy cancer. We asked why we can't do one or the other? Why do we need both? The doctor explained doing both is a one-two punch against the cancer -- together they are more effective than done alone.
Our next question was if the tumor should be removed before radiation and chemo. The doctor advised against it because he said radiation and chemo could shrink it or perhaps kill it all together. If it shrunk, less tissue would be destroyed removing it. Since it was surrounding a nerve, it was inoperable unless it shrunk off the nerve.
My loved one is claustrophobic so panic set in when viewing the radiation chamber. A net-like mask made specifically for the patient is used to bolt the patient down on the radiation platform keeping them immobile. You can see through the mask but you are aware you are trapped in it with no one present in the room for the length of the treatment. The radiation is mapped out and programmed so there can be no patient movement. My loved one was bolted down for ten minutes every weekday for seven weeks. A pill was taken to reduce the anxiety but it was still difficult. For the first two weeks, there was no difference in the appearance of the face, but eventually a severe sunburn appearance took hold. It is important that a cream is used anywhere the skin has been radiated to keep it from creating open fissures and peeling off. The radiated skin also tends to wrinkle up like it has been dehydrated unless it is moisturized. Hair around the nape of the neck was lost but has regrown. Wherever the most radiation is received, the hair follicles are destroyed. My loved one lost 90 percent hearing in one ear, one saliva gland, and taste has been altered. Chicken and many other things no longer taste good. Dry mouth will always be a problem and water must be available at all times to keep the mouth and throat wet.
The chemo therapy made my loved one very very sick. A lot of gagging and coughing up phlegm was experienced and sleep could only come one to two hours at a time before the gagging or nausea set in. Lying flat was impossible.
Twice during treatment my loved one experienced a hard ball forming on the face in a place other than the original cancer tumor. Was cancer growing in another nearby spot? Trips to the emergency room revealed an irritated salivary gland and an irritated lymph node -- not a new cancer.
My loved one hated the feeding tube and the liquid given to be used with it caused gas, nausea, and diarrhea. Liquid Ensure via the mouth was the meal of choice. A lot of weight was lost. A comfortable chair and bed near a bathroom is a necessity because there is a lot of fatigue, gagging and throwing up. Too much noise and activity around them causes irritation. However, they should not be left alone to dwell on their condition. They may be irritable, and unpleasant to be around, but still need to vent that irritation. It is best to just listen and let them vent. They need to have some control over their lives since cancer has taken away so much of it. The types of worries expressed can be concern over not being the person they were, that they are no longer useful or are a burden to their loved ones, and fear that they will be abandoned. At the same time that they are irritable, they may also be affectionate realizing that life is short and wanting to express their love while there is time. There may come a time when they do not want to talk about cancer because it is always present and they are weary from the battle. They just want to escape it for a while. If possible and they are up to it, arrange some excursion that distracts them from cancer and don’t mention cancer to them during that time.
My loved one has cancer but the whole family has it too…we are just experiencing it in a different way then the patient. For the first time you entertain life with the possibility that they won’t be in it. It seems impossible and unbearable. Little decisions seem so important because if the wrong treatment is given it could be disastrous, or your loved one could misunderstand what you are saying and be upset. Cancer is always the silent elephant in the room.
Tolerance for the way other family members cope with a loved one’s cancer is also needed. We don’t all react the same way. Just because someone acts strong does not mean they aren’t crying inside.
It’s difficult to sleep because of the flight/fight response you are experiencing in your desire to save your loved one. You may not want to talk about it with others because you have no answers to their questions and retelling the story is the same as reliving it.
After chemo and radiation, scans showed that the oral tumor shrank off the nerve leading to the brain but that cancer remained in the lymph nodes and thyroid in the neck. Extensive oral biopsy showed no cancer cells survived in the oral tumor area after treatment. No surgery was performed to remove anything in the mouth after chemo and radiation. There is a hard spot where the tumor was that may be scar tissue. Jaw mobility without pain was restored although the mouth cannot be opened as wide as before cancer. Some taste on one side of the tongue and some hearing returned. Fatigue remains.
THE MISTAKE WE MADE:
Why, after chemo and radiation, did cancer survive in the neck? It was a mystery until doctors realized my loved one had two different types of cancers at the same time, and they don't both respond to the same treatment. Make sure you are not the rare cancer patient that has more than one type of cancer that goes undetected while being treated for the one type of cancer that is known. Please do not make the mistake we did. We thought my loved one had cancer without realizing that there are many different types of cancers that respond to treatment differently. ==> Treatment for one type of cancer can render another type of cancer 'untreatable'! Because it is rare for a patient to have two types of cancer at once, the doctors treating my loved one did not realize there were two different cancers in play so they recommended a course of treatment for the cancer type they were aware of: Squamous Cell Cancer. The treatment as you know was radiation and chemotherapy followed by surgery.
Later, after radiation and chemotherapy, we found out that Thyroid cancer was also present. A scan revealed that because my loved one was radiated for the squamous cell cancer, the thyroid cancer cells have mutated into untreatable cancer cells. They can spread at will without being detected. A pet scan in some cases can find them but it is not reliable. This is not good news for us because we were relying on removing any cancer that spread and showed up during my loved one's lifetime. My loved one will continue with thyroid cancer treatment including lymph node and thyroid removal, which has been done, and swallowing a radioactive pill and remaining alone for five days. But there is no way to know if the pill will destroy all the thyroid cancer cells still present after surgery since they have mutated and are now resistant to treatment and undetectable.
When you have dental xrays, make sure your thyroid is shielded by the lead vest.
NECK SURGERY AND RESULTS TWO MONTHS AFTER SURGERY:
My loved one’s frontal neck surgery removed the thyroid and 40 lymph nodes of which 12 were cancerous with thyroid cancer -- not squamous cell like the tumor in the mouth. Lymph nodes in the rear of the neck were not touched and because of the prior radiation it cannot be determined if they are cancerous. Even though a daily thyroid medication is taken, my loved one has lost 60 pounds and is very thin. It is hard to tell if that is from the effects of the treatments or if a painful jaw is preventing proper levels of food consumption. For those concerned about scarring from this type of surgery, the scar extends from behind one ear down into the natural neck folds and up to behind the opposite ear in a smile formation.
The neck surgery took nine hours and was closed with staples which were removed painlessly after a week. Three draining tubes were inserted around the neck to drain the fluid buildup at the surgery site. They were removed two days after surgery (after two months, shoulder pain remains which is attributed to those tubes).
Massive doses of calcium are given during the hospital stay to see if the body is absorbing it post surgery. If the body absorbs correctly, the patient can go home to recover. My loved one spent four days in the hospital.
There was swelling in the neck area for a while but then it subsided and the neck looks normal. The neck is stiff and it became painful to hold up without support after surgery. No neck brace can be worn because of the surgical scar in that area. Eventually the neck muscles rebuild and it becomes easier to hold the neck and head up. Physical therapy is recommended because scar tissue can form that prevents neck mobility.
The scar is healing nicely but is still a very thin red smile line which is not that noticeable when looking straight frontal but is noticeable from the side view. The scar is expected to fade over time and does blend in nicely with the natural neck folds. The neck is slightly thinner but not deformed. It is important that a vitamin E cream is used on the scar after it closes and anywhere the skin has been radiated. The radiated skin tends to wrinkle up like it has been dehydrated unless it is moisturized. My loved one needs physical therapy to restore more function and movement to the neck but so far has refused. Without physical therapy and forced movement (even with some pain) scar tissue forms and muscle atrophy will eventually prevent mobility.
THE AFTER EFFECTS OF RADIATION AND CHEMO:
The radiation has caused jaw bone death which was expected around four months after radiation to the neck. My loved one underwent 20 rounds (1.5 hours each) in a hyperbolic chamber to force blood into the dying jaw area to stop the deterioration. During this process, an infection set in in the jaw and antibiotics had to be taken.
It has been weeks since we found out about the jaw bone death, and surgery was performed April 24, 2015 after 20 dives in the hyperbolic chamber. Because radiation to the face and neck tightens and changes the internal structures of the face and neck and makes resuscitation difficult, an air tube prior to surgery sometimes has to be inserted down the nose while the patient is awake prior to complete anesthesia. Luckily, my loved one had enough of an opening and jaw and neck movement that it was not necessary. A roughly 2.5 inch by 5 mm section of jaw bone and three teeth in the left lower rear jaw were removed during outpatient surgery. Blood was taken from my loved one, spun, and the growth factors removed from the blood. The growth factors were injected in the surgery site to induce the growth of blood vessels in the area since much tissue was damaged by the radiation to the side of the face and neck. The surgery took 3 hours from entering the operating room to recovery, and then my loved one went home to recover. Because morphine causes my loved one nightmares, Percocet was prescribed for pain. Even though an extra amount of numbing medication was administered at the end of surgery, pain at a level of 4 (from 1 to 10 with 10 being the worst) was experienced during recovery. Two Percocet, one at a time with a twenty minute wait time, was administered and helped tremendously. There will be a liquid diet the first two days and then a soft diet (scrambled eggs, macaroni and cheese, soups) for the next two weeks.
Ten more hyperbolic chamber dives of 1.5 hours each will be given now that the jaw surgery is complete in an effort to restore blood flow to the jaw.
It has been nearly three weeks since the jaw bone surgery and the ten hyperbolic chamber dives have been completed. The gums are not reattaching to the jaw bone as hoped and another section of dead bone has been found further back from the surgery site. Five more hyperbolic chamber dives are required before a course of treatment will be determined.
May 20, 2015 and the jawbone continues to die. The gums will not heal over the surgery site. No decisions on what to do yet. Wait, wait, wait another week for an answer. It could take a year or more before all the jaw bone that is going to die dies. In the meantime, infection is the immediate enemy. When the exposed dead jaw bone turns yellow, infection can set in and surgery must be performed. Always in the back of our minds is the question of how much jaw bone will be left and will it be disfiguring.
There is hope that the jawbone surgery will be the last surgery needed unless the cancer reappears and is detectable. But if the jaw bone surgery closes incorrectly, infection sets in, or the tissues do not regenerate, additional bone death can occur and more surgery will be required. If more jaw bone needs to be removed, bone will be taken from my loved one’s hip area to replace it. It is all a waiting game from now on.
It’s been a year now since that first cell mutated into cancer and all our lives are forever changed. Cancer is a bitch and it tests your metal in every conceivable way. Bless the oncologists, surgeons, nurses, and peripheral staff that fight this everyday on the front lines.
January 27, 2016. My loved one has had a full body scan that compared this scan with those of the past. It shows NO NEW incidences of cancer, or growth of cancer in previous cancerous areas. Hallelujah! There is a spot on the lung but that may just be a lesion from a previous infection. The next scan will be in six months. The jaw bone continues to deteriorate at the point it was radiated. The dry, brittle area is scraped off from time to time, but the gums stubbornly won't cover it. We are told we will have to wait to see how much jaw bone death will occur. My loved one, while looking well enough, still has lingering effects from chemo and radiation experiencing a tiredness and feeling old nearly a year after treatment. This is normal and may subside with time. There are intermittent sharp pains where the neck incision was made (from ear to ear) and the neck becomes sore and tires easily. My loved one mistakenly continues to refuse physical therapy for the neck and shoulder areas. The incision is no longer pink after a year and has receded nicely into the neck folds, although the cheek is dry and wrinkly from radiation. One doctor has recommended a filler under the skin for that area...not botox. Initially told incorrectly in May 2014 that this was Stage IV cancer, we are so grateful for this outcome to date, and look forward to increasingly better, less invasive, treatment for cancer.
May 9, 2016: Bad news…my loved one’s ultrasound found a 1cm lump on the left side of the neck. The doctors think it's a left over lymph node. My loved ones labs also came back with .2 on thyroid detection... which is low, but according to the doctors indicates thyroid cells are still in the body. My loved one may still have thyroid cancer. The next scan in five months will tell us more.
December 22, 2016: My loved one's two recent biopsies just came back negative for cancer! After radiation, chemo, multiple...too many to count.. hyperbolic chamber dives, dying jawbone, and three surgeries over two years...I'm so incredibly thankful! If you or a loved one has cancer, don't give up. Technology is on your side and winning more and more each day.
RESEARCH NOTES:
5/5/2015: My loved one was diagnosed with squamous cell oral cancer in 2014. Subsequently, after radiation and chemo for the oral cancer, thyroid cancer was found. We knew that there was cancer present in the neck before it was discovered to be thyroid cancer. We thought it was the squamous cell cancer that had spread from the oral tumor.
Why did my loved one have two cancers at the same time? Yes, it could be a coincidence, but one has to wonder if there is something more to it. My loved one had extensive fluoroscopy conducted after removal of uvula for sleep apnea, and swallowed barium during fluoroscopy xray to image the throat several years prior to developing cancer. Online research shows that the FDA was concerned as far back as 2008 about excessive radiation exposure in CT Scans. I am not recommending that anyone refuse a CT Scan or a fluoroscopy necessary for medical treatment, but there does seem to be evidence that cells subject to radiation can become damaged while remaining viable. With their mutated DNA, do they spawn cancer? After reading the articles below, it seems that many people develop leukemia (a blood cancer) years after receiving radiation. Unless I misunderstood the article, it seems a study done in 2008 in San Francisco indicated that not all medical x-rays had consistent levels of radiation, and many times the level of radiation was excessive. It was of enough concern, that the FDA posted a cancer risk notification on it's website.
These are the links I am referring to:
http://www.fda.gov/Radiation-EmittingProducts/RadiationEmittingProductsandPro cedures/MedicalImaging/MedicalX-Rays/ucm115354.htm
http://onlinelibrary.wiley.com/doi/10.3322/caac.21132/pdf
http://www.cancer.gov/cancertopics/causes/radiation/InterventionalFluor.pdf
4/15/2015: HOW IT WORKS: CANCER-FIGHTING IMMUNOTHERAPY
In the war against cancer, doctors have discovered a powerful new tool: the immune system. The FDA recently fast-tracked approval of three new immunotherapy drugs, called PD-1 inhibitors, designed to help white blood cells hunt down and eradicate hard-to-fight tumors--indefinitely. “Chemotherapy almost always stops working,” says Jonathan Cheng, executive director of oncology clinical development at Merck. “The promise of immune therapy is that you’re training the immune system to attack something foreign, so you’re able to maintain that activity for a very long time--hopefully for the rest of a patient’s life.”
Link: http://www.sciencehook.com/hook.php?entryID=360
4/15/2015: Cancer Research on the Evolution of Cancer Cells
Why does cancer go into remission after treatment, and then come roaring back? Cancer starts with one cell mutating in an abnormal way. Scientists mapping the evolution of cancer cells think there is evidence that cancer continues to mutate in stages and those stages do not respond to the same therapy. There may be cancer cells in a tumor in various stages of mutation so therapy will be effective for some parts of the tumor but not others. The tumor is like a family with many children (cells) at various ages that respond differently, e.g. you wouldn’t treat an infant the same as a five year old. Even though the tumor shrinks after treatment, some cancer cells within the tumor will be in a stage that makes them immune to that treatment. It is important that a tumor be analyzed to determine the stage that the majority of its cells are in to determine the most effective treatment. Through the 'evolutionary/family tree' line of research, scientists are hoping to change our ‘Cancer’ game from one of defense to offense. Read about it at: http://www.alwaysresearching.com/2015/04/15/from-snapshot-to-family-tree-writing-the-evolutionary-rule-book-of-cancer/?utm_source=dlvr.it&utm_medium=gplus
4/21/15 Pancreatic Cancer Research: A new research study has shown that pancreatic cancer cells can be coaxed to revert back toward normal cells by introducing a protein called E47. E47 binds to specific DNA sequences and controls genes involved in growth and differentiation. The research provides hope for a new treatment approach for the more than 40,000 people who die from the disease each year in the United States.
“For the first time, we have shown that overexpression of a single gene can reduce the tumor-promoting potential of pancreatic adenocarcinoma cells and reprogram them toward their original cell type. Thus, pancreatic cancer cells retain a genetic memory which we hope to exploit,” said Pamela Itkin-Ansari, Ph.D., adjunct professor in the Development, Aging, and Regeneration Program at Sanford-Burnham and lead author of the study published today in the journal Pancreas. E47 turns the clock back The study, a collaborative effort between Sanford-Burnham, UC San Diego, where Itkin-Ansari holds a joint appointment, and Purdue University, generated human pancreatic ductal adenocarcinoma cell lines to make higher-than-normal levels of E47. The increased amount of E47 caused cells to stall in the G0/G1 growth phase, and differentiate back toward an acinar cell phenotype. - See more at: http://beaker.sanfordburnham.org/2015/04/pancreatic-cancer-breakthrough-scientists-turn-cancer-cells-into-normal-cells/#sthash.oPYWrOHW.dpuf
April 27, 2015 Colon Rectal Cancer:
Author: Chris Jones-Cardiff
Cardiff University Original Study
Posted by Chris Jones-Cardiff on April 27, 2015
You are free to share this article under the Attribution 4.0 International license.
A new study is the first to show that common inherited genetic variants influence life expectancy in patients with colorectal cancer (CRC).
A team from Cardiff University’s School of Medicine analyzed over 7,600 patients with CRC from 14 different centers across the UK and the US. They found that a genetic variant in the gene CDH1 (encoding E-cadherin) was strongly linked to survival.
Having combined data of both inherited genetic variations and variations found within the cancers, the scientists believe that the resulting information will play a crucial role in managing patient survival.
“Our findings show that patients carrying a specific genetic variant, which is found in about 8 percent of patients, have worse survival, with a decrease in life expectancy of around four months in the advanced disease setting,” says study leader Professor Jeremy Cheadle.
“This work shows the potential use of genetic variants to help provide clinically useful information to patients suffering from colon cancer,” says Lee Campbell, science projects and research communications manager from Cancer Research Wales, which part-funded the study.
“Not only does this important piece of research allow clinicians to make more informed treatment decisions for individuals in future, but also has the capability to enhance existing screening or post-operative surveillance programs for this disease.”
“This represents a critical first step to improving colorectal cancer patient outcomes through a greater understanding of the influencing genetic factors,” adds Ian Lewis, director of research and policy at Tenovus Cancer Care.
The Bobby Moore Fund from Cancer Research UK, Tenovus Cancer Care, the Kidani Trust, Cancer Research Wales, and the National Institute for Social Care and Health Research Cancer Genetics Biomedical Research Unit (2011-2015) supported the work.
The findings are available in Clinical Cancer Research.
Source: Cardiff University
http://www.alwaysresearching.com/2015/04/27/gene-variant-linked-to-colon-cancer-survival/?utm_source=dlvr.it&utm_medium=gplus
Original article source: http://www.futurity.org/gene-bowel-colorectal-cancer-907542/
Clinical findings: http://clincancerres.aacrjournals.org/content/early/2015/04/14/1078-0432.CCR-14-3136.abstract
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July 7, 2017: What if curing cancer was as easy as getting an injection? That’s just what a pair of studies published this week in Nature tried to figure out.
The two teams of researchers conducted independent Phase I trials of personalized vaccines designed to prime the patients’ immune systems against melanomas, a category of skin cancers. In a scientific double whammy, both studies found that their vaccines—sometimes in combination with other immunotherapies—were able to prevent recurrence of the cancers in nearly all their subjects.
“We can safely and feasibly create a vaccine that is personalized to an individual’s tumor,” says Catherine Wu, senior author of one of the studies and associate professor at Dana-Farber Cancer Institute in Boston. “It’s not one-size-fits-all—rather, it’s tailored to the genetic composition of the patient’s tumor.”
Wu carried out her study with colleagues in Boston at Dana-Farber Cancer Institute and the Broad Institute. The other study was conducted in parallel by researchers in Germany, led by study first author Ugur Sahin, the co-founder and CEO of BioNTech, a biotechnology company that focuses on personalized immunotherapy treatments.
Both studies targeted the same type of cancer: melanoma. These skin cancers (best known for their link to UV radiation from tanning) are a good first target, Wu says, because scientists have a good understanding of the mutations that cause them. These mutations are the key, says Mathias Vormehr, a co-author on Sahin's study and a scientist at BioNTech.
"In principle, you can target any tumor that has mutations," Vormehr says. "And mutations are a main feature of tumors."
The goal of a cancer vaccine is to turn the patient's own immune system against the cancer by teaching it to fight the tumor cells. This is similar to other vaccines like the flu vaccine which contains dead or weakened flu viruses that can't actually do harm but can model what the the immune system should be prepared to fight.
Past attempts to create cancer vaccines have used gene-carrying viruses to reprogram immune cells to recognize cancerous cells. Others removed some immune cells from the patient's blood, taught them to recognize the cancer cells outside the body, then re-injected the trained immune cells into the patient to go to work.
The recent studies in Nature used neoantigen vaccines. Antigens are small proteins that decorate the outside of cells, and "neoantigens" refer to ones that are found only on cancer cells. Because they aren't found on any healthy cells, neoantigens make a perfect target for the immune system—after all, you wouldn’t want the immune system to start attacking its own healthy cells. Normally, cancer cells evade the immune system by weakening its effects and by feigning the appearance of normal cells. But, if the immune system learns to recognize the neoantigens delivered by the vaccine as harmful, it could then recognize and fight the cancer cells, too. Delivering mass amounts of neoantigens at once, which is what the vaccine would do, could trigger this recognition and the immune system might see neoantigens as harmful from then on.
Since all tumors are different, the vaccine had to be personalized. To figure out which neoantigens were unique to a patient's tumor, the researchers sequenced the tumor's DNA and each group of researchers developed their own computer algorithm to identify the unique segments of DNA that encoded the instructions to assemble these neoantigens.
This is the point where Wu and Sahin’s studies diverged. The goal was to get the neoantigens into the patient to prime their immune system. Wu’s team loaded up the vaccine with the neoantigens themselves, while Sahin’s vaccines delivered the corresponding RNA — a cellular intermediary between DNA and proteins—so that the patient's own cells could create the neoantigen. Sahin's team chose to use RNA because RNA serves a two-in-one role in the vaccine, Vormehr says. Vaccines normally have an added component that boosts the immune response, and RNA can accomplish that on its own.
(Remember that these cancer vaccines aren’t preventative, like the ones that you take for the flu. They are “therapeutic vaccines,” designed after the onset of cancer to target each individual’s tumor specifically.)
Both studies found that vaccination resulted in suppression of the cancer in many of their subjects. In the cases where the cancer was not successfully eliminated, Wu and Sahin both tried adding another treatment called checkpoint therapy, which keeps the cancerous cells from avoiding detection by the immune system. And two was, in fact, better than one: They found that the combination of the two methods improved vaccine response.
Of the six subjects in Wu’s study, four had stage III cancer and 25 months after vaccination, there was no sign of tumors. In the other two subjects, who had stage IV melanomas, they saw improvement with additional checkpoint therapy. Likewise, in Sahin’s study, eight out of 13 initially tumor-free subjects remained tumor-free 23 months later; normally half of them would be expected to relapse, Vormehr says. Of five subjects who relapsed, two responded positively to the vaccine, and a third responded when the vaccine was combined with checkpoint blockade therapy. Looking more closely, both sets of researchers found that their subjects' immune systems were learning to react to the neoantigens.
“Using very different delivery systems, we arrived at very similar conclusions,” Wu says. “It gives more robust grounds for proceeding into future directions.”
The purpose of the initial study was just to look for anti-tumor activity, says Matthias Miller, a senior project manager and co-author of the BioNTech study. In both cases, the trials were relatively small and did not have un-vaccinated control subjects. In a Nature News & Views piece that accompanied the two studies, Cornelis Melief, a professor at Leiden University Medical Center in the Netherlands who was not involved in either study, called for further Phase II clinical trials with larger samples and controls to more rigorously demonstrate the effectiveness of these vaccines.
One limitation of the studies was that not all cancer patients have neoantigen mutations that can be used to design these personalized vaccines, says Sasha Stanton, a physician-scientist in the University of Washington's Tumor Vaccine Group who was not involved in the study.
"Neoantigen vaccines are very exciting in metastatic cancer or in locally advanced cancer," Stanton says. "They are less beneficial in prevention and earlier stage cancer."
Additionally, the process is time intensive—for example, in Wu's study, it took three months for the patient to receive the vaccine—and not all patients can remain stable for that long, Stanton says. Production of the vaccine will also have to become more streamlined, Wu says, but she believes the timeframe can be brought down to 4-6 weeks. Miller is also optimistic about the accessibility of the BioNTech vaccine.
"It will be affordable," Miller says. "It can definitely reach the broader public upon improvement of the process."
BioNTech is working with Genentech, a pharmaceutical company, to further develop their vaccine, while Wu’s team is participating in a multi-center combination therapy trial sponsored by Neon Therapeutics, a pharmaceutical company founded by Wu. If future trials are successful, Wu says, there will be many opportunities to apply personalized vaccines to other types of cancer; glioblastoma, a type of brain cancer, is one possible target.
http://www.popsci.com/cancer-vaccines-immunotherapy?con=TrueAnthem&dom=tw&src=SOC&utm_campaign=&utm_content=5961f09404d30147867fac82&utm_medium=&utm_source=
The two teams of researchers conducted independent Phase I trials of personalized vaccines designed to prime the patients’ immune systems against melanomas, a category of skin cancers. In a scientific double whammy, both studies found that their vaccines—sometimes in combination with other immunotherapies—were able to prevent recurrence of the cancers in nearly all their subjects.
“We can safely and feasibly create a vaccine that is personalized to an individual’s tumor,” says Catherine Wu, senior author of one of the studies and associate professor at Dana-Farber Cancer Institute in Boston. “It’s not one-size-fits-all—rather, it’s tailored to the genetic composition of the patient’s tumor.”
Wu carried out her study with colleagues in Boston at Dana-Farber Cancer Institute and the Broad Institute. The other study was conducted in parallel by researchers in Germany, led by study first author Ugur Sahin, the co-founder and CEO of BioNTech, a biotechnology company that focuses on personalized immunotherapy treatments.
Both studies targeted the same type of cancer: melanoma. These skin cancers (best known for their link to UV radiation from tanning) are a good first target, Wu says, because scientists have a good understanding of the mutations that cause them. These mutations are the key, says Mathias Vormehr, a co-author on Sahin's study and a scientist at BioNTech.
"In principle, you can target any tumor that has mutations," Vormehr says. "And mutations are a main feature of tumors."
The goal of a cancer vaccine is to turn the patient's own immune system against the cancer by teaching it to fight the tumor cells. This is similar to other vaccines like the flu vaccine which contains dead or weakened flu viruses that can't actually do harm but can model what the the immune system should be prepared to fight.
Past attempts to create cancer vaccines have used gene-carrying viruses to reprogram immune cells to recognize cancerous cells. Others removed some immune cells from the patient's blood, taught them to recognize the cancer cells outside the body, then re-injected the trained immune cells into the patient to go to work.
The recent studies in Nature used neoantigen vaccines. Antigens are small proteins that decorate the outside of cells, and "neoantigens" refer to ones that are found only on cancer cells. Because they aren't found on any healthy cells, neoantigens make a perfect target for the immune system—after all, you wouldn’t want the immune system to start attacking its own healthy cells. Normally, cancer cells evade the immune system by weakening its effects and by feigning the appearance of normal cells. But, if the immune system learns to recognize the neoantigens delivered by the vaccine as harmful, it could then recognize and fight the cancer cells, too. Delivering mass amounts of neoantigens at once, which is what the vaccine would do, could trigger this recognition and the immune system might see neoantigens as harmful from then on.
Since all tumors are different, the vaccine had to be personalized. To figure out which neoantigens were unique to a patient's tumor, the researchers sequenced the tumor's DNA and each group of researchers developed their own computer algorithm to identify the unique segments of DNA that encoded the instructions to assemble these neoantigens.
This is the point where Wu and Sahin’s studies diverged. The goal was to get the neoantigens into the patient to prime their immune system. Wu’s team loaded up the vaccine with the neoantigens themselves, while Sahin’s vaccines delivered the corresponding RNA — a cellular intermediary between DNA and proteins—so that the patient's own cells could create the neoantigen. Sahin's team chose to use RNA because RNA serves a two-in-one role in the vaccine, Vormehr says. Vaccines normally have an added component that boosts the immune response, and RNA can accomplish that on its own.
(Remember that these cancer vaccines aren’t preventative, like the ones that you take for the flu. They are “therapeutic vaccines,” designed after the onset of cancer to target each individual’s tumor specifically.)
Both studies found that vaccination resulted in suppression of the cancer in many of their subjects. In the cases where the cancer was not successfully eliminated, Wu and Sahin both tried adding another treatment called checkpoint therapy, which keeps the cancerous cells from avoiding detection by the immune system. And two was, in fact, better than one: They found that the combination of the two methods improved vaccine response.
Of the six subjects in Wu’s study, four had stage III cancer and 25 months after vaccination, there was no sign of tumors. In the other two subjects, who had stage IV melanomas, they saw improvement with additional checkpoint therapy. Likewise, in Sahin’s study, eight out of 13 initially tumor-free subjects remained tumor-free 23 months later; normally half of them would be expected to relapse, Vormehr says. Of five subjects who relapsed, two responded positively to the vaccine, and a third responded when the vaccine was combined with checkpoint blockade therapy. Looking more closely, both sets of researchers found that their subjects' immune systems were learning to react to the neoantigens.
“Using very different delivery systems, we arrived at very similar conclusions,” Wu says. “It gives more robust grounds for proceeding into future directions.”
The purpose of the initial study was just to look for anti-tumor activity, says Matthias Miller, a senior project manager and co-author of the BioNTech study. In both cases, the trials were relatively small and did not have un-vaccinated control subjects. In a Nature News & Views piece that accompanied the two studies, Cornelis Melief, a professor at Leiden University Medical Center in the Netherlands who was not involved in either study, called for further Phase II clinical trials with larger samples and controls to more rigorously demonstrate the effectiveness of these vaccines.
One limitation of the studies was that not all cancer patients have neoantigen mutations that can be used to design these personalized vaccines, says Sasha Stanton, a physician-scientist in the University of Washington's Tumor Vaccine Group who was not involved in the study.
"Neoantigen vaccines are very exciting in metastatic cancer or in locally advanced cancer," Stanton says. "They are less beneficial in prevention and earlier stage cancer."
Additionally, the process is time intensive—for example, in Wu's study, it took three months for the patient to receive the vaccine—and not all patients can remain stable for that long, Stanton says. Production of the vaccine will also have to become more streamlined, Wu says, but she believes the timeframe can be brought down to 4-6 weeks. Miller is also optimistic about the accessibility of the BioNTech vaccine.
"It will be affordable," Miller says. "It can definitely reach the broader public upon improvement of the process."
BioNTech is working with Genentech, a pharmaceutical company, to further develop their vaccine, while Wu’s team is participating in a multi-center combination therapy trial sponsored by Neon Therapeutics, a pharmaceutical company founded by Wu. If future trials are successful, Wu says, there will be many opportunities to apply personalized vaccines to other types of cancer; glioblastoma, a type of brain cancer, is one possible target.
http://www.popsci.com/cancer-vaccines-immunotherapy?con=TrueAnthem&dom=tw&src=SOC&utm_campaign=&utm_content=5961f09404d30147867fac82&utm_medium=&utm_source=
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Cancer treatments in development - Using bull sperm called Spermbots to deliver chemotherapy directly to cancerous cells! Using bee venom to deliver chemotherapy through the brain barrier to brain cancer. Using viruses as chemo delivery agents. Read on:
Cancer patients are all too familiar with the debilitating effects of chemotherapy, still a mainstay of treatment for many malignancies. But as some researchers work to find new drugs, others are working to create new drug-delivery tools. Some of that work involves hacking things like virus particles and bee venom— even sperm cells.
The goal of the research is to find ways to target the delivery of cancer drugs more effectively in order to boost their effectiveness and alleviate side effects— which in some cases are no less dangerous than the cancer itself.
“Some chemotherapy drugs can destroy patients’ hearts or kidneys,” says Daniel Kohane, a Harvard Medical School professor whose lab conducts research on biomaterials and drug delivery.
Chemotherapy works essentially by killing fast-growing cells. But cancer cells aren’t the only ones in the body that reproduce rapidly. Cells in the intestinal lining turn over quickly. Ditto for hair follicles and blood cells. So as chemo takes on cancer cells, it’s also damaging healthy cells.
“Only about 0.1 percent of the drug molecules actually reach and go into the tumors,” says Haifa Shen, an associate professor of nanomedicine at the Houston Methodist Research Institute who studies drug delivery methods. “Over 99.9 percent of chemo drug molecules stay outside of the tumors, being very toxic to normal tissues.”
Viruses vs. Breast Cancer
Viruses are promising drug-delivery tools because, once inside the body, they’re great at finding their way to specific types of cells while avoiding other types. Cold viruses target cells lining the nose, throat, and lungs, for example, while the Ebola virus attacks cells in the liver and arteries. Once inside their target cells, viruses unload their cargo of genetic material and set the stage for the production of more virus particles.
It would be a major advance in cancer therapy if researchers could find a way to modify viruses so as to retain their targeting capabilities while swapping out their genetic cargo for potent anticancer molecules. And Frank Sainsbury and his team at the University of Queensland in Australia are doing just that. In a series of preliminary experiments, the scientists created “fake” viruses whose outer shells, or capsids, were engineered to attach only to breast cancer cells.
“It’s somewhat similar to how two magnets interact with each other, and we can build the capsid’s surface that way,” Sainsbury says.
Sainsbury started off with Bluetongue, a virus that affects only cows and sheep. Using tobacco plants as incubators, the team created empty Bluetongue capsids and then loosed them on breast cancer cells in a petri dish. The shells did what the scientists hoped they would. They found their targets, and the cancer cells “took them in,” according to Sainsbury.
Bluetongue shells make good drug delivery vehicles because they can carry a lot. “They are big shells with a lot of cargo space that we can fill with drug molecules,” Sainsbury says. He added that the next step for his research will be to load the shells with chemo drugs and get them to unload their cargo to kill tumors.
Modified Bee Venom
Cancers vary in lethality, and brain cancer is often a death sentence— in part because few drugs are able to reach the brain.
The brain is separated from the rest of the body by a protective membrane that keeps out microbes, viruses, and other potentially harmful organisms and substances. “Your brain is like a medieval city surrounded by stonewalls with the guards at the gates that select who can go through,” says Ernest Giralt, a professor of organic chemistry at the University of Barcelona in Spain. “So very few chemicals can get into the brain.”
Luckily, some substances are able to sneak in. One is bee venom, or apamin, which bees release when they sting.
In its original form, apamin can’t be used therapeutically because it harms nerve cells. So Giralt’s team chemically modified apamin to take away the molecule’s toxic effects. The team injected mice with the modified apamin and observed no side effects. And the modified apamin crossed the brain membrane even more easily than the original version. “It was pure serendipity,” Giralt says.
The team is now exploring the best way to use apamin to shuttle chemo drugs into the brain. There seem to be two ways to do it, Giralt says. One would be simply to attach a chemo molecule to modified apamin. The other would be to fashion a sort of “bulk shipment”— basically stashing a load of chemo into a virus shell studded with apamin molecules and testing whether it can pass through the membrane.
‘Spermbots’ to the Rescue
Hardly anyone would think of sperm as a tool to fight cancer, but a group of researchers at IFW Dresden and Chemnitz University of Technology in Germany did. Their preliminary research suggests that it might be possible to turn sperm into “sperm-hybrid micromotors” able to deliver chemotherapy agents to malignancies of the cervix, ovaries, or uterus.
Sperm, of course, have evolved to navigate the female reproductive tract. They neither damage tissue nor cause toxic side effects. To create the spermbots, the scientists soaked bull sperm cells in the cancer drug doxorubicin and then “dressed” the cells with tiny iron-coated mesh. Then they used magnets to steer the cells toward tumor cells in a petri dish.
Three days later, only 13 percent of tumor cells were still alive–a level of effectiveness far superior to that seen when doxorubicin was delivered without spermbots.
The scientists foresee a day in which patients with gynecological cancers might lie inside a magnetic chamber where an electromagnetic field would direct the sperm cells to their target. “It would be somewhat similar to lying inside an MRI machine,” says Haifeng Xu, lead author of a paper describing the research.
June 2017
https://futurism.com/spermbots-have-come-to-aid-us-in-the-war-against-cancer/
Cancer patients are all too familiar with the debilitating effects of chemotherapy, still a mainstay of treatment for many malignancies. But as some researchers work to find new drugs, others are working to create new drug-delivery tools. Some of that work involves hacking things like virus particles and bee venom— even sperm cells.
The goal of the research is to find ways to target the delivery of cancer drugs more effectively in order to boost their effectiveness and alleviate side effects— which in some cases are no less dangerous than the cancer itself.
“Some chemotherapy drugs can destroy patients’ hearts or kidneys,” says Daniel Kohane, a Harvard Medical School professor whose lab conducts research on biomaterials and drug delivery.
Chemotherapy works essentially by killing fast-growing cells. But cancer cells aren’t the only ones in the body that reproduce rapidly. Cells in the intestinal lining turn over quickly. Ditto for hair follicles and blood cells. So as chemo takes on cancer cells, it’s also damaging healthy cells.
“Only about 0.1 percent of the drug molecules actually reach and go into the tumors,” says Haifa Shen, an associate professor of nanomedicine at the Houston Methodist Research Institute who studies drug delivery methods. “Over 99.9 percent of chemo drug molecules stay outside of the tumors, being very toxic to normal tissues.”
Viruses vs. Breast Cancer
Viruses are promising drug-delivery tools because, once inside the body, they’re great at finding their way to specific types of cells while avoiding other types. Cold viruses target cells lining the nose, throat, and lungs, for example, while the Ebola virus attacks cells in the liver and arteries. Once inside their target cells, viruses unload their cargo of genetic material and set the stage for the production of more virus particles.
It would be a major advance in cancer therapy if researchers could find a way to modify viruses so as to retain their targeting capabilities while swapping out their genetic cargo for potent anticancer molecules. And Frank Sainsbury and his team at the University of Queensland in Australia are doing just that. In a series of preliminary experiments, the scientists created “fake” viruses whose outer shells, or capsids, were engineered to attach only to breast cancer cells.
“It’s somewhat similar to how two magnets interact with each other, and we can build the capsid’s surface that way,” Sainsbury says.
Sainsbury started off with Bluetongue, a virus that affects only cows and sheep. Using tobacco plants as incubators, the team created empty Bluetongue capsids and then loosed them on breast cancer cells in a petri dish. The shells did what the scientists hoped they would. They found their targets, and the cancer cells “took them in,” according to Sainsbury.
Bluetongue shells make good drug delivery vehicles because they can carry a lot. “They are big shells with a lot of cargo space that we can fill with drug molecules,” Sainsbury says. He added that the next step for his research will be to load the shells with chemo drugs and get them to unload their cargo to kill tumors.
Modified Bee Venom
Cancers vary in lethality, and brain cancer is often a death sentence— in part because few drugs are able to reach the brain.
The brain is separated from the rest of the body by a protective membrane that keeps out microbes, viruses, and other potentially harmful organisms and substances. “Your brain is like a medieval city surrounded by stonewalls with the guards at the gates that select who can go through,” says Ernest Giralt, a professor of organic chemistry at the University of Barcelona in Spain. “So very few chemicals can get into the brain.”
Luckily, some substances are able to sneak in. One is bee venom, or apamin, which bees release when they sting.
In its original form, apamin can’t be used therapeutically because it harms nerve cells. So Giralt’s team chemically modified apamin to take away the molecule’s toxic effects. The team injected mice with the modified apamin and observed no side effects. And the modified apamin crossed the brain membrane even more easily than the original version. “It was pure serendipity,” Giralt says.
The team is now exploring the best way to use apamin to shuttle chemo drugs into the brain. There seem to be two ways to do it, Giralt says. One would be simply to attach a chemo molecule to modified apamin. The other would be to fashion a sort of “bulk shipment”— basically stashing a load of chemo into a virus shell studded with apamin molecules and testing whether it can pass through the membrane.
‘Spermbots’ to the Rescue
Hardly anyone would think of sperm as a tool to fight cancer, but a group of researchers at IFW Dresden and Chemnitz University of Technology in Germany did. Their preliminary research suggests that it might be possible to turn sperm into “sperm-hybrid micromotors” able to deliver chemotherapy agents to malignancies of the cervix, ovaries, or uterus.
Sperm, of course, have evolved to navigate the female reproductive tract. They neither damage tissue nor cause toxic side effects. To create the spermbots, the scientists soaked bull sperm cells in the cancer drug doxorubicin and then “dressed” the cells with tiny iron-coated mesh. Then they used magnets to steer the cells toward tumor cells in a petri dish.
Three days later, only 13 percent of tumor cells were still alive–a level of effectiveness far superior to that seen when doxorubicin was delivered without spermbots.
The scientists foresee a day in which patients with gynecological cancers might lie inside a magnetic chamber where an electromagnetic field would direct the sperm cells to their target. “It would be somewhat similar to lying inside an MRI machine,” says Haifeng Xu, lead author of a paper describing the research.
June 2017
https://futurism.com/spermbots-have-come-to-aid-us-in-the-war-against-cancer/
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A 3D animation showing how cancer cells spread to other parts of the body.
https://www.youtube.com/watch?v=rrMq8uA_6iA
https://www.youtube.com/watch?v=rrMq8uA_6iA
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June 28, 2017 - This is one of many promising cancer treatments on the horizon that could mark the end of the prevalence of the second biggest killer in the U.S. Recently, the FDA has fast-tracked testing of Pembrolizumab (branded Keytruda), which significantly shrunk and stabilized tumors in 66 of 86 test patients. A new test, backed by Bill Gates and Jeff Bezos, has been discovered that has significant potential in diagnosing cancer. These all could be tools for extending human lifespan and reducing suffering in our world.
A new study has found that laser-heated gold nanorods have the potential to "burn the legs" off cancer cells and decrease levels of the protein that causes their rapid growth. This, along with other recent discoveries, has the potential to help millions of people.
A GOLDEN METHOD
Researchers in Georgia have used laser-heated gold nanorods to disable the mechanism cancer cells use to spread to other sites in the body (a process called metastasis) — which is “the primary cause of cancer-related deaths,” the researchers wrote in the study recently published in PNAS.
Precisely, the method works by attacking the lamellipodia and filopodia — aspects of the cell’s cytoskeleton that act like legs, allowing it to migrate. When cells turn cancerous, production of lamellipodia and filopodia can go into overdrive.
The gold rods inhibited this transportation mechanism in two ways. First, the rods were armed with molecules that attracted and trapped the cellular machinery that caused the overproduction of lamellipodia and filopodia. Second, the rods were heated with a low energy laser of infrared light. Moustafa Ali, first author on the study, said in an interview for a Georgia Tech press release, “the light was not absorbed by the cells, but the gold nanorods absorbed it, and as a result, they heated up and partially melted cancer cells they are connected with, mangling lamellipodia and filopodia.”
A POSSIBLE END TO CANCER?
The new method has not been tested in humans yet, so many more studies must be done. But, if shown to be effective, it has the potential to help millions. The American cancer society predicts that, in 2017 alone, 1,688,780 new cancer cases will be diagnosed, and 600,920 people will die from the disease.
The gold nanorods have the most potential to help head, neck, breast, and skin cancer sufferers in particular, as the ideal depth for the laser to heat the nanorod is two to three centimeters (about an inch) beneath the skin’s surface. It is an especially attractive option promising because it is less invasive than current treatments.
It would also not harm healthy cells, making it a preferable treatment to chemotherapy, which often kills cells without discrimination. It would have reduced risk for toxic side effects, and — due to its mildness — could likely be used repeatedly.
References: Gatech, American Cancer Society , Medical News Today
https://futurism.com/scientists-have-discovered-a-way-to-burn-the-legs-off-cancer/
A new study has found that laser-heated gold nanorods have the potential to "burn the legs" off cancer cells and decrease levels of the protein that causes their rapid growth. This, along with other recent discoveries, has the potential to help millions of people.
A GOLDEN METHOD
Researchers in Georgia have used laser-heated gold nanorods to disable the mechanism cancer cells use to spread to other sites in the body (a process called metastasis) — which is “the primary cause of cancer-related deaths,” the researchers wrote in the study recently published in PNAS.
Precisely, the method works by attacking the lamellipodia and filopodia — aspects of the cell’s cytoskeleton that act like legs, allowing it to migrate. When cells turn cancerous, production of lamellipodia and filopodia can go into overdrive.
The gold rods inhibited this transportation mechanism in two ways. First, the rods were armed with molecules that attracted and trapped the cellular machinery that caused the overproduction of lamellipodia and filopodia. Second, the rods were heated with a low energy laser of infrared light. Moustafa Ali, first author on the study, said in an interview for a Georgia Tech press release, “the light was not absorbed by the cells, but the gold nanorods absorbed it, and as a result, they heated up and partially melted cancer cells they are connected with, mangling lamellipodia and filopodia.”
A POSSIBLE END TO CANCER?
The new method has not been tested in humans yet, so many more studies must be done. But, if shown to be effective, it has the potential to help millions. The American cancer society predicts that, in 2017 alone, 1,688,780 new cancer cases will be diagnosed, and 600,920 people will die from the disease.
The gold nanorods have the most potential to help head, neck, breast, and skin cancer sufferers in particular, as the ideal depth for the laser to heat the nanorod is two to three centimeters (about an inch) beneath the skin’s surface. It is an especially attractive option promising because it is less invasive than current treatments.
It would also not harm healthy cells, making it a preferable treatment to chemotherapy, which often kills cells without discrimination. It would have reduced risk for toxic side effects, and — due to its mildness — could likely be used repeatedly.
References: Gatech, American Cancer Society , Medical News Today
https://futurism.com/scientists-have-discovered-a-way-to-burn-the-legs-off-cancer/
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Alzheimer’s disease affects about 5.5 million Americans — a number that’s expected to balloon to 13.8 million by 2050.
As the most common cause of dementia, it’s the sixth leading cause of death in the US, behind conditions like heart disease and cancer.
The growing number of people who have the disease is troubling, because there are only four approved drugs that treat symptoms of the disease, and several hopeful treatments have failed key studies in 2017.
==> Unexpectedly, it’s something researchers at the top cancer hospital in the US are looking into. While cancer and Alzheimer’s seemingly don’t have that much in common, there is one key link that researchers at MD Anderson think could be useful: People with a history of cancer are less likely to get Alzheimer’s, while people with Alzheimer’s are less likely to get cancer.
“Age is the biggest risk factor for both. But then for some reason, some people go one direction, others go another direction,” Jim Ray, head of research for the Neurodegeneration Consortium at MD Anderson told Business Insider.
==>In the last decade the researchers have made this observational link between the development of Alzheimer’s and a decreased cancer risk and vice versa. So researchers have been hypothesizing why that happens. At a very simplified level, the cause of the diseases might hold the biggest clue. “Cancer is a disease of cells that cannot die, will not die. Alzheimer’s is a disease of cells that are supposed to live your entire lifetime that you can’t keep alive,” he said.
One of the ways researchers have been getting clues into the link is in cancer patients who have chemotherapy-related cognitive dysfunction. An estimated 75% of cancer patients have some level of cognitive impairment (memory loss, attention problems, etc.). Chemotherapy works by killing cancer cells by targeting fast-dividing cells, and in most cases, kills off some healthy cells along the way, including nerve cells in the brain.
“It’s an understudied area,” Ray said. “And I think a lot of people didn’t fully realize it was a problem.”
It’s something drug researchers have started looking into, to see if there could be a therapy that prevents the neurological damage that happens with chemotherapy. If they can figure out what’s going on and how to prevent the neurological side effects for cancer patients, the same approach could hold some promise in treating Alzheimer’s as well.
New Ways to Tackle Alzheimer’s
The search for new Alzheimer’s treatments hasn’t been going well. The last new drug approved was back in 2003, and a slew of failed trials in the beginning of 2017 has cast a shadow over the field.
Still, more drugs are in late-stage trials that could have an impact on the disease, and researchers are pinning hopes on diagnosing the disease early, before symptoms even show up. If any of those treatments pan out, it could change the way we look at the disease and potentially make the statistics a lot less dire.
Unlike some of the promising treatments that have failed in 2017 that deal with the so-called “amyloid hypothesis” (the treatments target amyloid beta deposits in the brain that accumulate in people with Alzheimer’s disease), approaches that try to prevent nerve cells from dying wouldn’t have any impact on that buildup. Instead of trying to clear the body of the deposits, it would just try to strengthen the nerve cells that are there.
“What we’re trying to do is make your nerve cells more resistant to damage,” Ray said. “It won’t stop the damage, but it’d just make them more resistant longer, be more resilient.
June 30, 2017
https://futurism.com/theres-a-weird-relationship-between-cancer-and-alzheimers/
As the most common cause of dementia, it’s the sixth leading cause of death in the US, behind conditions like heart disease and cancer.
The growing number of people who have the disease is troubling, because there are only four approved drugs that treat symptoms of the disease, and several hopeful treatments have failed key studies in 2017.
==> Unexpectedly, it’s something researchers at the top cancer hospital in the US are looking into. While cancer and Alzheimer’s seemingly don’t have that much in common, there is one key link that researchers at MD Anderson think could be useful: People with a history of cancer are less likely to get Alzheimer’s, while people with Alzheimer’s are less likely to get cancer.
“Age is the biggest risk factor for both. But then for some reason, some people go one direction, others go another direction,” Jim Ray, head of research for the Neurodegeneration Consortium at MD Anderson told Business Insider.
==>In the last decade the researchers have made this observational link between the development of Alzheimer’s and a decreased cancer risk and vice versa. So researchers have been hypothesizing why that happens. At a very simplified level, the cause of the diseases might hold the biggest clue. “Cancer is a disease of cells that cannot die, will not die. Alzheimer’s is a disease of cells that are supposed to live your entire lifetime that you can’t keep alive,” he said.
One of the ways researchers have been getting clues into the link is in cancer patients who have chemotherapy-related cognitive dysfunction. An estimated 75% of cancer patients have some level of cognitive impairment (memory loss, attention problems, etc.). Chemotherapy works by killing cancer cells by targeting fast-dividing cells, and in most cases, kills off some healthy cells along the way, including nerve cells in the brain.
“It’s an understudied area,” Ray said. “And I think a lot of people didn’t fully realize it was a problem.”
It’s something drug researchers have started looking into, to see if there could be a therapy that prevents the neurological damage that happens with chemotherapy. If they can figure out what’s going on and how to prevent the neurological side effects for cancer patients, the same approach could hold some promise in treating Alzheimer’s as well.
New Ways to Tackle Alzheimer’s
The search for new Alzheimer’s treatments hasn’t been going well. The last new drug approved was back in 2003, and a slew of failed trials in the beginning of 2017 has cast a shadow over the field.
Still, more drugs are in late-stage trials that could have an impact on the disease, and researchers are pinning hopes on diagnosing the disease early, before symptoms even show up. If any of those treatments pan out, it could change the way we look at the disease and potentially make the statistics a lot less dire.
Unlike some of the promising treatments that have failed in 2017 that deal with the so-called “amyloid hypothesis” (the treatments target amyloid beta deposits in the brain that accumulate in people with Alzheimer’s disease), approaches that try to prevent nerve cells from dying wouldn’t have any impact on that buildup. Instead of trying to clear the body of the deposits, it would just try to strengthen the nerve cells that are there.
“What we’re trying to do is make your nerve cells more resistant to damage,” Ray said. “It won’t stop the damage, but it’d just make them more resistant longer, be more resilient.
June 30, 2017
https://futurism.com/theres-a-weird-relationship-between-cancer-and-alzheimers/
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Recognizing cancer cells in the body and capturing them in the bloodstream - June 27, 2017 - Cancerous tumors are formidable enemies, recruiting blood vessels to aid their voracious growth, damaging nearby tissues, and deploying numerous strategies to evade the body's defense systems. But even more malicious are the circulating tumor cells (CTCs) that tumors release, which travel stealthily through the bloodstream and take up residence in other parts of the body, a process known as metastasis. While dangerous, their presence is also a valuable indicator of the stage of a patient's disease, making CTCs an attractive new approach to cancer diagnostics. Unfortunately, finding the relative handful of CTCs among the trillions of healthy blood cells in the human body is like playing the ultimate game of needle-in-a-haystack: CTCs can make up as few as one in ten thousand of the cells in the blood of a cancer patient. This is made even more difficult by the lack of broad-spectrum CTC capture agents, as the most commonly used antibodies fail to recognize many types of cancer cells.
To address this problem, a group of researchers at the Wyss Institute at Harvard University has adapted an engineered human blood opsonin protein known as FcMBL, which was originally developed as a broad-spectrum pathogen capture agent, to target CTCs instead. Using magnetic beads coated with FcMBL, they were able to capture >90% of seven different types of cancer cells. "We were able to rapidly isolate CTCs both in vitro and from blood, including some which are not bound by today's standard CTC-targeting technologies," says Michael Super, Ph.D., Lead Senior Staff Scientist at the Wyss Institute and co-author of the paper. "This new technique could become useful in cancer diagnostics." The technology is described today in Advanced Biosystems.
Current CTC diagnostic systems frequently make use of a cancer cell marker, the epithelial cell adhesion molecule (EpCAM), which is highly expressed on the surface of tumor cells. However, EpCAM expression on cancer cells decreases when tumor cells transform into CTCs, ironically making EpCAM-based tests less useful precisely when it is most crucial to know that a patient's cancer has metastasized.
The Wyss Institute capture technology takes advantage of a protein naturally found in the body, mannose-binding lectin (MBL), which recognizes and binds to carbohydrates present on the surfaces of bacteria and other pathogens, marking them for destruction by the immune system. Healthy human cells have different carbohydrate patterns and are immune to MBL, but many cancer cells have aberrant carbohydrates that are similar to those found on pathogens and, therefore, are vulnerable to MBL binding.
The team previously developed a genetically engineered version of MBL in which the binding portion is fused to an antibody Fc fragment (FcMBL) to stabilize the molecule. Past studies showed that when tiny magnetic beads are coated with FcMBL and added to various pathogens, the FcMBL-coated beads attach to the surfaces of these cells like flies on flypaper so that, when a magnetic field is applied, the beads drag their bound cells along with them toward the magnet.
To evaluate whether this system could specifically target CTCs, the researchers implanted fluorescently-labeled human breast cancer cells in mice, let the tumors develop for 28 days, and then tested the blood to determine the number of CTCs present. They then mixed the blood with FcMBL-coated beads and pulled the beads out of suspension with a magnet. "The FcMBL-coated beads are unlikely to be bound to normal cells, and so when we measured the movement of cancer cells versus normal cells, the cancer cells moved much faster because they were being dragged to the magnet by the beads," explains first author Joo Kang, Ph.D., who was a Technology Development Fellow at the Wyss Institute while completing this study and is now an Assistant Professor at the Ulsan National Institute of Science and Technology. The concentration of CTCs present in the blood was also reduced by more than 93%, showing that FcMBL can effectively capture CTCs in the blood even after they have undergone the transitions that reduce EpCAM expression.
The team then tested their system against six additional cancer cell types, including human non-small cell lung cancer, lung carcinoma, and glioblastoma. The FcMBL-coated beads captured all six types of tumor cells with >90% efficiency - which is comparable to EpCAM-targeting methods - and were also able to capture two types that are not successfully bound by anti-EpCAM antibodies (lung carcinoma and glioblastoma). "Our results suggest that while the EpCAM marker can be useful for some tumors, it becomes less and less useful over time as EpCAM expression decreases and the cell becomes metastatic," says Super. "Our FcMBL system can either be used as an alternative to EpCAM-based diagnostics, or as a follow-up method once EpCAM ceases to be expressed."
The researchers hope to continue their studies to determine exactly which carbohydrate molecules FcMBL is targeting on CTCs, which could further improve the specificity and efficacy of capture. "The FcMBL opsonin technology has already been shown to be an extremely broad-spectrum capture agent for pathogens," says senior author of the study and Wyss Founding Director Donald Ingber, who is also the Judah Folkman Professor of Vascular Biology at Harvard Medical School (HMS) and the Vascular Biology Program at Boston Children's Hospital, as well as a Professor of Bioengineering at Harvard's School of Engineering and Applied Sciences. "This new finding that it has similar broad-spectrum binding activity for many different types of circulating cancer cells is equally exciting, and once again demonstrates the power of leveraging biological design principles when developing new medical innovations."
Read more at: https://medicalxpress.com/news/2017-06-weapon-war-cancer.html#jCp
To address this problem, a group of researchers at the Wyss Institute at Harvard University has adapted an engineered human blood opsonin protein known as FcMBL, which was originally developed as a broad-spectrum pathogen capture agent, to target CTCs instead. Using magnetic beads coated with FcMBL, they were able to capture >90% of seven different types of cancer cells. "We were able to rapidly isolate CTCs both in vitro and from blood, including some which are not bound by today's standard CTC-targeting technologies," says Michael Super, Ph.D., Lead Senior Staff Scientist at the Wyss Institute and co-author of the paper. "This new technique could become useful in cancer diagnostics." The technology is described today in Advanced Biosystems.
Current CTC diagnostic systems frequently make use of a cancer cell marker, the epithelial cell adhesion molecule (EpCAM), which is highly expressed on the surface of tumor cells. However, EpCAM expression on cancer cells decreases when tumor cells transform into CTCs, ironically making EpCAM-based tests less useful precisely when it is most crucial to know that a patient's cancer has metastasized.
The Wyss Institute capture technology takes advantage of a protein naturally found in the body, mannose-binding lectin (MBL), which recognizes and binds to carbohydrates present on the surfaces of bacteria and other pathogens, marking them for destruction by the immune system. Healthy human cells have different carbohydrate patterns and are immune to MBL, but many cancer cells have aberrant carbohydrates that are similar to those found on pathogens and, therefore, are vulnerable to MBL binding.
The team previously developed a genetically engineered version of MBL in which the binding portion is fused to an antibody Fc fragment (FcMBL) to stabilize the molecule. Past studies showed that when tiny magnetic beads are coated with FcMBL and added to various pathogens, the FcMBL-coated beads attach to the surfaces of these cells like flies on flypaper so that, when a magnetic field is applied, the beads drag their bound cells along with them toward the magnet.
To evaluate whether this system could specifically target CTCs, the researchers implanted fluorescently-labeled human breast cancer cells in mice, let the tumors develop for 28 days, and then tested the blood to determine the number of CTCs present. They then mixed the blood with FcMBL-coated beads and pulled the beads out of suspension with a magnet. "The FcMBL-coated beads are unlikely to be bound to normal cells, and so when we measured the movement of cancer cells versus normal cells, the cancer cells moved much faster because they were being dragged to the magnet by the beads," explains first author Joo Kang, Ph.D., who was a Technology Development Fellow at the Wyss Institute while completing this study and is now an Assistant Professor at the Ulsan National Institute of Science and Technology. The concentration of CTCs present in the blood was also reduced by more than 93%, showing that FcMBL can effectively capture CTCs in the blood even after they have undergone the transitions that reduce EpCAM expression.
The team then tested their system against six additional cancer cell types, including human non-small cell lung cancer, lung carcinoma, and glioblastoma. The FcMBL-coated beads captured all six types of tumor cells with >90% efficiency - which is comparable to EpCAM-targeting methods - and were also able to capture two types that are not successfully bound by anti-EpCAM antibodies (lung carcinoma and glioblastoma). "Our results suggest that while the EpCAM marker can be useful for some tumors, it becomes less and less useful over time as EpCAM expression decreases and the cell becomes metastatic," says Super. "Our FcMBL system can either be used as an alternative to EpCAM-based diagnostics, or as a follow-up method once EpCAM ceases to be expressed."
The researchers hope to continue their studies to determine exactly which carbohydrate molecules FcMBL is targeting on CTCs, which could further improve the specificity and efficacy of capture. "The FcMBL opsonin technology has already been shown to be an extremely broad-spectrum capture agent for pathogens," says senior author of the study and Wyss Founding Director Donald Ingber, who is also the Judah Folkman Professor of Vascular Biology at Harvard Medical School (HMS) and the Vascular Biology Program at Boston Children's Hospital, as well as a Professor of Bioengineering at Harvard's School of Engineering and Applied Sciences. "This new finding that it has similar broad-spectrum binding activity for many different types of circulating cancer cells is equally exciting, and once again demonstrates the power of leveraging biological design principles when developing new medical innovations."
Read more at: https://medicalxpress.com/news/2017-06-weapon-war-cancer.html#jCp
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Note: Metformin, which has been shown to prevent cancer and extend life in animals, began clinical testing as an anti-aging drug in February 2017! In October 2016, molecular geneticist Jan Vijg published a paper claiming that the human lifespan was limited to 115 years. This kindled a vigorous controversy among scientists, and on June 28 of this year, five groups of scientists published formal rebuttals to the claim.
Vijg’s work analyzed demographic data from the 20th century, taken all over the world, and demonstrated that peak age plateaued at about 115 years starting in the mid-1990s. Based on their results, the authors concluded that the natural human age limit is 115 years old and that there is the probability of less than 1 in 10,000 of living to be more than 125 years old.
You could probably guess, not everyone in the scientific community agrees. Most criticisms arise from the way the Vijg team handled their data, and their process for drawing conclusions. First, the Vijg team tested their data to prove whether or not the plateau they felt they observed after 1995 was in fact present. In other words, they generated a hypothesis and then tested it using the same dataset, which is typically unacceptable, as it causes inaccurate results due to severe overfitting, a fit based on error or noise, not a real relationship.
Second, the team’s actual data set was very small because in each year they counted only the oldest person who died. They then subjected this inordinately small sample to standard linear regression techniques, which was not appropriate based both on the small sample size, and the additional fact that the individuals being counted were outliers who should have been subject to extreme event analysis. In fact, the decline suggested in the 2016 conclusions appears to be suggested by a single death in the data set.
Moreover, other scientists reanalyzed the data and found it consistent with multiple lifespan trajectories, not just the one reported in 2016. Finally, several scientists in their rebuttals point to the overall body of work on the biology of aging over the past few decades which suggests that the human lifespan has been far more flexible than previously believed; which alone indicates that the proposed limit should be viewed with extreme caution.
TAKEAWAYS FROM THE CONTROVERSY
The authors of the original study stand by their work and disagree with the criticisms of the statistical methods used. Vijg also believes that the real cause of the outcry is not the data, which is convincing, but the fact that aging can’t be stopped and there is a limit to human life: “I guess the main message is that a lot of people have difficulty accepting that everything now points toward an end in the increase of maximum lifespan,” Vijg told The Scientist.
University of Illinois at Chicago professor of public health Jay Olshansky, who was involved in neither the original study nor the rebuttals, thinks the criticizing scientists are missing the real point of the 2016 study, which he clarified for The Scientist: “The most important message to get across, in my view, is that we should not be trying to make ourselves live longer, we should only be trying to extend the period of healthy life.”
However, there are many others pushing the limits of human longevity right now who disagree strongly enough to put their money where their philosophy is. Since research has demonstrated that transfusions of younger blood, or parabiosis, was able to rehabilitate cognitive abilities in mice, a startup called Ambrosia has started to offer a human clinical trial of parabiosis for paying clients. Peter Diamandis of the genotype research facility, Human Longevity, Inc., is searching for the key to using nanomachines or stem cells to regenerate our bodies. And Metformin, which has been shown to prevent cancer and extend life in animals, began clinical testing as an anti-aging drug in February.
There are so many possibilities in motion that it does seem hard to agree with a firm limit to the human lifespan. In the end, time will resolve the controversy once and for all. Ironically, we’ll only be here to see it if the critics are right.
https://futurism.com/there-may-be-no-limits-to-how-long-humans-can-live/
Vijg’s work analyzed demographic data from the 20th century, taken all over the world, and demonstrated that peak age plateaued at about 115 years starting in the mid-1990s. Based on their results, the authors concluded that the natural human age limit is 115 years old and that there is the probability of less than 1 in 10,000 of living to be more than 125 years old.
You could probably guess, not everyone in the scientific community agrees. Most criticisms arise from the way the Vijg team handled their data, and their process for drawing conclusions. First, the Vijg team tested their data to prove whether or not the plateau they felt they observed after 1995 was in fact present. In other words, they generated a hypothesis and then tested it using the same dataset, which is typically unacceptable, as it causes inaccurate results due to severe overfitting, a fit based on error or noise, not a real relationship.
Second, the team’s actual data set was very small because in each year they counted only the oldest person who died. They then subjected this inordinately small sample to standard linear regression techniques, which was not appropriate based both on the small sample size, and the additional fact that the individuals being counted were outliers who should have been subject to extreme event analysis. In fact, the decline suggested in the 2016 conclusions appears to be suggested by a single death in the data set.
Moreover, other scientists reanalyzed the data and found it consistent with multiple lifespan trajectories, not just the one reported in 2016. Finally, several scientists in their rebuttals point to the overall body of work on the biology of aging over the past few decades which suggests that the human lifespan has been far more flexible than previously believed; which alone indicates that the proposed limit should be viewed with extreme caution.
TAKEAWAYS FROM THE CONTROVERSY
The authors of the original study stand by their work and disagree with the criticisms of the statistical methods used. Vijg also believes that the real cause of the outcry is not the data, which is convincing, but the fact that aging can’t be stopped and there is a limit to human life: “I guess the main message is that a lot of people have difficulty accepting that everything now points toward an end in the increase of maximum lifespan,” Vijg told The Scientist.
University of Illinois at Chicago professor of public health Jay Olshansky, who was involved in neither the original study nor the rebuttals, thinks the criticizing scientists are missing the real point of the 2016 study, which he clarified for The Scientist: “The most important message to get across, in my view, is that we should not be trying to make ourselves live longer, we should only be trying to extend the period of healthy life.”
However, there are many others pushing the limits of human longevity right now who disagree strongly enough to put their money where their philosophy is. Since research has demonstrated that transfusions of younger blood, or parabiosis, was able to rehabilitate cognitive abilities in mice, a startup called Ambrosia has started to offer a human clinical trial of parabiosis for paying clients. Peter Diamandis of the genotype research facility, Human Longevity, Inc., is searching for the key to using nanomachines or stem cells to regenerate our bodies. And Metformin, which has been shown to prevent cancer and extend life in animals, began clinical testing as an anti-aging drug in February.
There are so many possibilities in motion that it does seem hard to agree with a firm limit to the human lifespan. In the end, time will resolve the controversy once and for all. Ironically, we’ll only be here to see it if the critics are right.
https://futurism.com/there-may-be-no-limits-to-how-long-humans-can-live/
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Veterans Affairs Taps Energy Department’s Supercomputers for Big Data Health Projects - May 23, 2017 - The two departments teamed up to analyze health data from veterans for genomic and cancer research. What do you get when you match the Veterans Affairs Department’s data with the Energy Department’s supercomputers? Powerful insights.
At least that’s what the two departments are hoping. Earlier this month they announced a partnership called the VA-DOE Big Data Science Initiative, which will be based within DOE’s National Laboratory system, one of the world’s top resources for supercomputing.
Under the initiative, the agencies will analyze large sets of digital health and genomic data from the VA and other federal sources. The goal is to improve the health of veterans and others in areas such as suicide prevention, cancer and heart disease, while also spurring DOE’s next-generation supercomputing designs.
VA has the data and DOE has the technological expertise in Big Data analytics, artificial intelligence and high-performance computing. DOE claims that its supercomputers are “capable of millions of billions of calculations per second.” Combined, the two hope to identify trends that will support the development of new treatments and preventive strategies, the agencies said in a statement.
Secure Supercomputing to Help Veterans
Over the past two decades, the VA has collected health data trend information from roughly 24 million veterans who have used VA for healthcare, according to a statement from VA Secretary Dr. David Shulkin.
“We are partnering with DOE to use their high-performance computing capabilities to allow thousands of researchers access to this unprecedented data resource over time in a secure environment,” he said in a statement. “The transformative science that will be developed through this partnership will improve health care for veterans and all Americans.”
VA said it “takes privacy seriously and has ensured all reasonable safeguards are in place to protect the records at the DOE National Laboratory.” However, the agency did not detail the specific security measures it is putting in place to protect the data that will be used in the initiative.
One program the two agencies will push forward is known as “MVP-CHAMPION,” short for the Million Veteran Program (MVP) Computational Health Analytics for Medical Precision to Improve Outcomes Now.
MVP, VA’s innovative genomics program, has already enrolled more than 560,000 veteran volunteers, who have provided DNA samples; completed surveys about their health, lifestyle and military experiences; and granted secure access to their electronic health records for research purposes. The agencies say the new partnership “will maximize the impact of studies using MVP data.”
After the partnership was announced, Energy Secretary Rick Perry, a former U.S. Air Force pilot, donated blood as part of the MVP initiative. “It’s important to provide a good example for the Secretary of Energy to be engaged in the program,” Perry said at an event in Houston last week, according to the Houston Chronicle. “There are a lot of good reasons to be involved in this program — having that level of expertise taking a look at your DNA; giving you insight into what to be on the lookout for; continuing volunteering to help improve care for the next generation of servicemen and women.”
Analyzing Veterans’ Data for Multiple Projects
The new VA-DOE program will use data from MVP and VA’s electronic health records system, as well as health data from the Defense Department, the Centers for Medicare and Medicaid Services, and the Centers for Disease Control’s National Death Index.
The VA and Energy Department have already mapped out an initial suite of specific studies that are part of the Big Data Science Initiative.
One aims to “build algorithms to generate highly tailored personalized risk scores for suicide,” according to a statement. The VA said last year that about 20 veterans commit suicide per day.
According to the agencies, the scores could be used by VA clinicians and researchers to help predict which patients are at highest risk for suicide and to evaluate prevention strategies. The researchers will work with VA’s Office of Suicide Prevention to enhance current algorithms already in use in the VA, according to the VA and DOE.
Meanwhile, another project will focus on prostate cancer and “will seek new ways to tell which tumors are lethal versus nonlethal cancer and require treatment, and, by contrast, others that are slow-growing and unlikely to cause any symptoms.”
The initiative will also explore “what sets of risk factors are the best predictors of certain forms of cardiovascular disease to inform individualized therapy and treatments for patients based on their individual risk factors.”
http://www.fedtechmagazine.com/article/2017/05/veterans-affairs-taps-energy-department-s-supercomputers-big-data-health-projects
At least that’s what the two departments are hoping. Earlier this month they announced a partnership called the VA-DOE Big Data Science Initiative, which will be based within DOE’s National Laboratory system, one of the world’s top resources for supercomputing.
Under the initiative, the agencies will analyze large sets of digital health and genomic data from the VA and other federal sources. The goal is to improve the health of veterans and others in areas such as suicide prevention, cancer and heart disease, while also spurring DOE’s next-generation supercomputing designs.
VA has the data and DOE has the technological expertise in Big Data analytics, artificial intelligence and high-performance computing. DOE claims that its supercomputers are “capable of millions of billions of calculations per second.” Combined, the two hope to identify trends that will support the development of new treatments and preventive strategies, the agencies said in a statement.
Secure Supercomputing to Help Veterans
Over the past two decades, the VA has collected health data trend information from roughly 24 million veterans who have used VA for healthcare, according to a statement from VA Secretary Dr. David Shulkin.
“We are partnering with DOE to use their high-performance computing capabilities to allow thousands of researchers access to this unprecedented data resource over time in a secure environment,” he said in a statement. “The transformative science that will be developed through this partnership will improve health care for veterans and all Americans.”
VA said it “takes privacy seriously and has ensured all reasonable safeguards are in place to protect the records at the DOE National Laboratory.” However, the agency did not detail the specific security measures it is putting in place to protect the data that will be used in the initiative.
One program the two agencies will push forward is known as “MVP-CHAMPION,” short for the Million Veteran Program (MVP) Computational Health Analytics for Medical Precision to Improve Outcomes Now.
MVP, VA’s innovative genomics program, has already enrolled more than 560,000 veteran volunteers, who have provided DNA samples; completed surveys about their health, lifestyle and military experiences; and granted secure access to their electronic health records for research purposes. The agencies say the new partnership “will maximize the impact of studies using MVP data.”
After the partnership was announced, Energy Secretary Rick Perry, a former U.S. Air Force pilot, donated blood as part of the MVP initiative. “It’s important to provide a good example for the Secretary of Energy to be engaged in the program,” Perry said at an event in Houston last week, according to the Houston Chronicle. “There are a lot of good reasons to be involved in this program — having that level of expertise taking a look at your DNA; giving you insight into what to be on the lookout for; continuing volunteering to help improve care for the next generation of servicemen and women.”
Analyzing Veterans’ Data for Multiple Projects
The new VA-DOE program will use data from MVP and VA’s electronic health records system, as well as health data from the Defense Department, the Centers for Medicare and Medicaid Services, and the Centers for Disease Control’s National Death Index.
The VA and Energy Department have already mapped out an initial suite of specific studies that are part of the Big Data Science Initiative.
One aims to “build algorithms to generate highly tailored personalized risk scores for suicide,” according to a statement. The VA said last year that about 20 veterans commit suicide per day.
According to the agencies, the scores could be used by VA clinicians and researchers to help predict which patients are at highest risk for suicide and to evaluate prevention strategies. The researchers will work with VA’s Office of Suicide Prevention to enhance current algorithms already in use in the VA, according to the VA and DOE.
Meanwhile, another project will focus on prostate cancer and “will seek new ways to tell which tumors are lethal versus nonlethal cancer and require treatment, and, by contrast, others that are slow-growing and unlikely to cause any symptoms.”
The initiative will also explore “what sets of risk factors are the best predictors of certain forms of cardiovascular disease to inform individualized therapy and treatments for patients based on their individual risk factors.”
http://www.fedtechmagazine.com/article/2017/05/veterans-affairs-taps-energy-department-s-supercomputers-big-data-health-projects
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From the link below: The TAPUR study by ASCO - At Cancer Treatment Centers of America® (CTCA), genomic medicine plays a prominent role in our commitment to delivering innovative, personalized treatments to our patients. The TAPUR clinical trial offers an important new approach. “This trial changes the entire language of clinical research in cancer. Rather than base treatments on large populations of patients, the study looks at the individual patient's tumor. This is the future of cancer research. It changes the thought processes for how oncologists treat cancer.”
The Targeted Agent and Profiling Utilization Registry (TAPUR) study is a clinical trial that aims to improve our understanding of how commercially available anti-cancer drugs perform on a broader range of cancers, by matching the drugs to tumors with specific genomic mutations that the drugs are designed to target. CTCA enrolls qualified patients at all five of our hospitals.
The trial, led by the American Society of Clinical Oncology (ASCO), will collect data on the drugs’ effectiveness, adverse side effects and other patient outcomes, providing insights that may lead to new uses for approved drugs.
While the targeted therapies under study have been approved by the U.S. Food and Drug Administration (FDA) to treat specific cancers, this trial will collect data on how the drugs perform on patients with cancer types that they are not yet approved to treat. Such treatments, used outside their FDA-approved indications, are often not covered by insurance companies, putting the drugs out of reach of many patients and physicians. By actively studying these drugs, which are provided at no cost to the study participant, the trial aims to offer new insights on the drugs’ potential uses.
"What we have here is not just one drug or one molecular abnormality. We have multiple molecular abnormalities, multiple drugs, multiple companies participating in this trial,” says Dr. Maurie Markman, President of Medicine & Science at CTCA. “This ASCO-led trial focuses on what we can find within an individual patient's cancer that can help identify a new treatment option.”
The TAPUR trial data will be collected in an extensive database, and results will be widely shared, potentially benefiting the cancer community, federal regulators and the drug makers alike.
Who is involved?
As part of the study, seven pharmaceutical companies are making 17 anti-cancer drugs available at no cost to participating patients. Qualified candidates are those with advanced cancer who meet the eligibility criteria, who have exhausted conventional treatment options and whose genomic test reveals a tumor mutation that may be targeted with an anti-cancer drug made available in the trial, as long as the drug has not been approved for their cancer type. For a full listing of participating companies, please go to TAPUR.org.
Hospitals around the country, including all five CTCA hospitals, are enrolling patients. At CTCA, our cancer experts recognize the promise of precision cancer treatment and are proud to offer this comprehensive clinical trial to qualifying patients.
Do I qualify for participation?
Generally speaking, qualifying participants must:
Be 18 or older
Not be pregnant or planning to become pregnant during the trial timeline
Not be bed-ridden
Have been diagnosed with an advanced solid tumor, multiple myeloma or B cell non-Hodgkin lymphoma
Have exhausted available standard treatment options
Have had a genomic or molecular test performed on their tumor
Have genomic test results that reveal their tumor has a mutation that may be targeted with a drug included in the trial and not approved for that cancer type
In other words, if the trial includes a targeted therapy approved to treat melanoma and designed to attack a specific mutation, a lung cancer patient with that mutation would qualify, but a melanoma patient with the same mutation would not, because the drug is already approved for this therapy.
Why now?
The genomic medicine era
The science of cancer care is changing, moving to a truly personalized, precision approach, and this trial is part of an effort to uncover evidence-based insights that may lead to new, individualized treatments. Traditionally, cancer treatments attack the disease based on where it appears in the body: Breast cancer treatments are for cancers that develop in the breast; lung cancer treatments attack cancers in the lung.
Advances in cancer research have broadened our understanding of the disease, on a molecular level, leading to the potential for a more targeted, precision approach—a core element of the CTCA approach to cancer care.
Now, advanced genomic tests on some tumors are used to map out the cancer’s DNA profile, revealing abnormalities that may be responsible for driving the malignancy’s growth and behavior. Scientists are discovering that common mutations are found across cancer types, meaning that several patients may have the same mutation, even though their cancers were found in different areas of the body. Some lung cancers may look and behave like breast cancers with the same mutation, for example—and both may benefit from the same treatment.
Today’s generation of targeted therapies is designed to favorably impact these mutations, known as “actionable genomic variants.” Recent studies on patients with advanced cancer suggest these variants are found in 20 percent to 40 percent of tumors, according to ASCO’s TAPUR website. But the field is still evolving, and the cancer world is hungry for more data on how these drugs perform on more cancer types.
At CTCA, advanced genomic testing of certain tumors is integral to our commitment to providing our patients with innovative, precision cancer treatment options. The TAPUR trial offers an exciting opportunity, for the science of cancer care in general and our patients in particular, to learn more about how those drugs perform on more cancer types.
What is special about TAPUR?
There are several reasons the CTCA and cancer community at large are excited about the TAPUR trial’s possibilities:
It may lead to more treatment options. This trial aims to amass a broad pool of data that may help uncover new uses for existing drugs in more cancer types, based on specific abnormalities.
It’s truly precision medicine. Rather than targeting all cells in the body, hoping to impact the cancer cells most, precision medicine identifies the specific mutations that cause a specific type of cancer to develop. TAPUR is testing drugs that the FDA has concluded are safe and effective to treat specific mutations in specific cancer types. The TAPUR study aims to learn whether using these drugs in other cancer types with the same mutations will also yield safe and effective therapies. Therefore, TAPUR focuses on the mutations and is open to a wide range of cancer types.
It is more inclusive. Unlike studies with very rigid qualifications for eligibility, this trial is designed to include a wider patient population. As a result, TAPUR is learning from the experience of a wider array of cancer patients.
"This is the future of cancer research," says Dr. Markman. "It cannot be overstated how important this trial is. It changes the trajectory, the future, the thought processes for how oncologists treat cancer.”
Have questions?
To learn more about the TAPUR trial, how to determine eligibility and how to enroll for participation in the trial at a CTCA hospital, call (855) 781-5864. If you are onsite at one our hospitals, please visit the Precision Medicine Center for more information.
http://www.cancercenter.com/ctca-difference/tapur/?invsrc=paid_social&utm_budget=corp&utm_campaign=tapur_trial&utm_channel=social&utm_site=twitter
The Targeted Agent and Profiling Utilization Registry (TAPUR) study is a clinical trial that aims to improve our understanding of how commercially available anti-cancer drugs perform on a broader range of cancers, by matching the drugs to tumors with specific genomic mutations that the drugs are designed to target. CTCA enrolls qualified patients at all five of our hospitals.
The trial, led by the American Society of Clinical Oncology (ASCO), will collect data on the drugs’ effectiveness, adverse side effects and other patient outcomes, providing insights that may lead to new uses for approved drugs.
While the targeted therapies under study have been approved by the U.S. Food and Drug Administration (FDA) to treat specific cancers, this trial will collect data on how the drugs perform on patients with cancer types that they are not yet approved to treat. Such treatments, used outside their FDA-approved indications, are often not covered by insurance companies, putting the drugs out of reach of many patients and physicians. By actively studying these drugs, which are provided at no cost to the study participant, the trial aims to offer new insights on the drugs’ potential uses.
"What we have here is not just one drug or one molecular abnormality. We have multiple molecular abnormalities, multiple drugs, multiple companies participating in this trial,” says Dr. Maurie Markman, President of Medicine & Science at CTCA. “This ASCO-led trial focuses on what we can find within an individual patient's cancer that can help identify a new treatment option.”
The TAPUR trial data will be collected in an extensive database, and results will be widely shared, potentially benefiting the cancer community, federal regulators and the drug makers alike.
Who is involved?
As part of the study, seven pharmaceutical companies are making 17 anti-cancer drugs available at no cost to participating patients. Qualified candidates are those with advanced cancer who meet the eligibility criteria, who have exhausted conventional treatment options and whose genomic test reveals a tumor mutation that may be targeted with an anti-cancer drug made available in the trial, as long as the drug has not been approved for their cancer type. For a full listing of participating companies, please go to TAPUR.org.
Hospitals around the country, including all five CTCA hospitals, are enrolling patients. At CTCA, our cancer experts recognize the promise of precision cancer treatment and are proud to offer this comprehensive clinical trial to qualifying patients.
Do I qualify for participation?
Generally speaking, qualifying participants must:
Be 18 or older
Not be pregnant or planning to become pregnant during the trial timeline
Not be bed-ridden
Have been diagnosed with an advanced solid tumor, multiple myeloma or B cell non-Hodgkin lymphoma
Have exhausted available standard treatment options
Have had a genomic or molecular test performed on their tumor
Have genomic test results that reveal their tumor has a mutation that may be targeted with a drug included in the trial and not approved for that cancer type
In other words, if the trial includes a targeted therapy approved to treat melanoma and designed to attack a specific mutation, a lung cancer patient with that mutation would qualify, but a melanoma patient with the same mutation would not, because the drug is already approved for this therapy.
Why now?
The genomic medicine era
The science of cancer care is changing, moving to a truly personalized, precision approach, and this trial is part of an effort to uncover evidence-based insights that may lead to new, individualized treatments. Traditionally, cancer treatments attack the disease based on where it appears in the body: Breast cancer treatments are for cancers that develop in the breast; lung cancer treatments attack cancers in the lung.
Advances in cancer research have broadened our understanding of the disease, on a molecular level, leading to the potential for a more targeted, precision approach—a core element of the CTCA approach to cancer care.
Now, advanced genomic tests on some tumors are used to map out the cancer’s DNA profile, revealing abnormalities that may be responsible for driving the malignancy’s growth and behavior. Scientists are discovering that common mutations are found across cancer types, meaning that several patients may have the same mutation, even though their cancers were found in different areas of the body. Some lung cancers may look and behave like breast cancers with the same mutation, for example—and both may benefit from the same treatment.
Today’s generation of targeted therapies is designed to favorably impact these mutations, known as “actionable genomic variants.” Recent studies on patients with advanced cancer suggest these variants are found in 20 percent to 40 percent of tumors, according to ASCO’s TAPUR website. But the field is still evolving, and the cancer world is hungry for more data on how these drugs perform on more cancer types.
At CTCA, advanced genomic testing of certain tumors is integral to our commitment to providing our patients with innovative, precision cancer treatment options. The TAPUR trial offers an exciting opportunity, for the science of cancer care in general and our patients in particular, to learn more about how those drugs perform on more cancer types.
What is special about TAPUR?
There are several reasons the CTCA and cancer community at large are excited about the TAPUR trial’s possibilities:
It may lead to more treatment options. This trial aims to amass a broad pool of data that may help uncover new uses for existing drugs in more cancer types, based on specific abnormalities.
It’s truly precision medicine. Rather than targeting all cells in the body, hoping to impact the cancer cells most, precision medicine identifies the specific mutations that cause a specific type of cancer to develop. TAPUR is testing drugs that the FDA has concluded are safe and effective to treat specific mutations in specific cancer types. The TAPUR study aims to learn whether using these drugs in other cancer types with the same mutations will also yield safe and effective therapies. Therefore, TAPUR focuses on the mutations and is open to a wide range of cancer types.
It is more inclusive. Unlike studies with very rigid qualifications for eligibility, this trial is designed to include a wider patient population. As a result, TAPUR is learning from the experience of a wider array of cancer patients.
"This is the future of cancer research," says Dr. Markman. "It cannot be overstated how important this trial is. It changes the trajectory, the future, the thought processes for how oncologists treat cancer.”
Have questions?
To learn more about the TAPUR trial, how to determine eligibility and how to enroll for participation in the trial at a CTCA hospital, call (855) 781-5864. If you are onsite at one our hospitals, please visit the Precision Medicine Center for more information.
http://www.cancercenter.com/ctca-difference/tapur/?invsrc=paid_social&utm_budget=corp&utm_campaign=tapur_trial&utm_channel=social&utm_site=twitter
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