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Michael Castro
Works at Personalized Cancer Medicine, PLLC
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Michael Castro

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How should we respond?- Aspirin Use, Tumor PIK3CA Mutation, and Colorectal-Cancer Survival Liao et al, N Engl J Med 2012; 367:1596-1606
 
It’s commonly known amongst news anchors and their viewing audiences that aspirin protects against various forms of cancer.  Several years ago, Andrew Chan and the group at Mass. General Hospital reported a 49% decrease in death rate among patients with metastatic colorectal cancer who use aspirin regularly. (JAMA. 2009;302(6):649-658) In the subset whose cancers express COX2 (now renamed prostaglandin-endoperoxide synthase 2 PTGS2), a known biomarker for aggressive disease and adverse outcome, the reduction in mortality was 61%, a larger magnitude of mortality reduction than from our best cytotoxic drugs.   Without COX2 expression, there was no benefit.  Notably, these observations have been pretty well ignored by guideline makers and clinicians because they are retrospective.  In the meantime, one diagnostics company that used to sell COX2 tissue assays stopped doing so because of criticism from medical oncologists for recommending ASA. 
 
This week we learn an even better way of identifying which patients benefit from ASA, and the benefit is compelling.  Dr. Xiaoyun Liao from MGH reported on 82% reduction in mortality among ASA users who possess PIK3CA mutations and no benefit at all amongst PIK3CA wild type patients.  When all patients were considered together, the risk reduction was 54%, pretty impressive because PIK3CA was only mutated in 17%.  But the survival prolongation in mutant group was so large that the average benefit for the entire group was still enormous.  In fact, only 2/62 (3%) ASA users died within 5 years compared to 23/90 (26%) who did not take ASA.
 
 
Is this study practice changing in the official sense of moving the standard of care?  Not really.  Since it was retrospective, the finding does not prove beyond a shadow of a doubt that taking aspirin as a cancer specific intervention among patients PIK3CA mutant disease is helpful.  The accompanying editorial from Boris Pasche  reflects this view, but may be a much too conservative response to these data.  In fact, the statistical analysis of reduction in death rate attributed to ASA tells us that the likelihood this occurred by chance is < 1/1000. 
 
As patient advocates, we must consider the consequences of taking a conservative position and failing to offer a virtually life saving benefit.  After all, by the time a prospective randomized trial is convened, completed, and reported, many would die a lot faster from being deprived of ASA.  This makes the case for early adoption: either put everyone on ASA, or do the test for PIK3CA mutation to see who really needs it.  Anything less neglects one of the most profound therapeutic insights ever for combating an aggressive form of disease.  After all, PIK3CA upregulates the AKT pathway, and this blocks apoptosis, the capacity of tumor cells to die.  Patients with this molecular aberration respond less well to treatment and have shorter survivals.  We should be gleeful that we can block this biology, and  for virtually no cost at all.  I would even advocate PIK3CA testing in the adjuvant setting.   We may not be on incontrovertible turf with this practice, but I would argue we don’t need to be since the error of being overly conservative leads to preventable deaths for patients.
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Gimmick turns into advance: the approval of Abraxane for NSCLC should SPARC your interest.
 
When paclitaxel (Taxol) came to the end of its patent life, the drug was re-invented by encapsulating it inside of an albumin nanoparticle  NAB-paclitaxel (Abraxane) rather than dissolving paclitaxel in cremaphor, the tree sap derivative associated with severe and some times life-threatening hypersensitivity reactions.  Elimination of infusion reactions and the need for premedication with high dose dexamethasone, antihistamines, and H-2 blockers was an interesting “gimmick” in re-patenting a workhorse drug and keeping the revenues high for industry.
 
Subsequently, secreted protein acidic and rich in cysteine (SPARC) was found to be present in a wide variety of human cancers.  SPARC modulates cell-cell and cell matrix interactions, and usually is associated with aggressive biological behavior.   SPARC turns out to be an electrical sink for albumin, which is “consumed” by cancer cells in a process referred to as autophagy.   Autophagy probably accounts for cachexia in cancer and has recently led to clinical trials of chloroquine to inhibit the process. 
 
In 2006, data emerged from the head and neck literature that SPARC positive tumors have a response rate to Abraxane of 78% compared to 25% in SPARC negative patients resulting from the enhanced drug delivery to cancer cells.  Also, Abraxane appears to be the most active agent available for treating SPARC positive pancreatic cancer.
 
Nevertheless, in the old-fashioned population style method of assuming all patients are the same, head-to-head trials in lung cancer between Abraxane and paclitaxel were pursued.  They show superior response rates for Abraxane: squamous-cell tumors (41% versus 24%) and those with large-cell carcinoma (33% versus 15%). Undoubtedly, SPARC expression accounts for the superior activity, yet the drug is now labeled for NSCLC in general.  
 
The one size fits all approach will likely lead to the over-utilization of an expensive drug for roughly half of patients who are SPRAC negative and derive no incremental value over paclitaxel alone.  On the other hand, for the SPARC positive subset Abraxane results in superior anti-tumor activity and yields two-three times the efficacy of vanilla paclitaxel.   Certainly, oncologists are capable of making this simple distinction, which is not only good for patients, but also leads to savings in the health care dollar.
 
What about adenocarcinoma? The two regimens produced equivalent response rates in patients with adenocarcinoma histology (26% versus 27%). Yet the new FDA label for Abraxane includes adenocarcinoma, since the study was not designed to distinguish lung cancer histologies.  This is good for the drug company’s revenues, but does not really advance the best interests of patients or the health care system.  Profiling for SPARC expression can yield to a far more intelligent utilization of resources.
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Platinum-based adjuvant chemotherapy may be harmful in lung cancer with KRAS exon 13 mutations.
 
Prognostic and predictive effects of KRAS mutation subtype in completely resected non-small cell lung cancer (NSCLC): A LACE-bio study.  Shepherd F, et al.  Pro ASCO 2012, Abstract 7007
 
There was a fascinating retrospective biomarker study presented at the cancer meetings last June looking back at 1532 patients who were randomized to observation or standard platinum-based treatment.  Usually we expect about a 14% reduction in the hazard rate (HR) for death from chemotherapy.  This study looked at the impact of KRAS mutations on outcome.  Distressingly, the HR for death actually increased dramatically in patients whose cancers harbored an exon 13 mutations (HR 5.78, p=0.001) as a result of chemotherapy.  This was not the case for exon 12 mutations where a variety of statistically insignificant trends were observed - some in favor and some against the benefit of treatment.  The adverse impact is not because KRAS exon 13 patients do worse in general, since in the observation arm, there was no difference in survival between KRAS WT, exon 12 and exon 13 mutations.  Therefore, this really does appear to be a theranostic marker for harm from treatment.  It is also fascinating that not all mutations are created equal.  The genomic revolution will thus continue to challenge our wishes that oncology could be easy.
 
How do we apply retrospective data in the daily practice of medical oncology?  Some would say not at all.  But I would say that these data deserve more attention: they reveal a large tendency towards harm, and the study itself was based on a well done placebo-controlled randomized trial.  After all, the absolute survival benefit from chemotherapy is only 4%, but a nearly 6-fold increase in the chance of dying from chemotherapy should sound an alarm.
 
On the other hand, molecular profiling can, Identify who can derive a larger than usual survival benefit from platinum based therapy in patients without exon 13 mutations.  Thus, molecular profiling allows for a stronger recommendation for chemotherapy for reluctant or marginal patient.  At the same time, patients who might not benefit or actually be harmed can find support from their doctors when they are who are strongly predisposed against receiving chemotherapy.  For patients with KRAS exon13(+) disease desiring adjuvant therapy, clinical trial options become extremely important in the treatment planning process.  There are a few alternative on the drawing board that might significantly help this group.
 
Molecular profiling is not currently part of patient management in this disease.  But I would suggest that we should adopt profiling so that we can begin to individualize and improve the informed consent process and use the latest insights to get the results we want.
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Attacking the hedgehog pathway: another strategy for avoiding cytotoxic therapy in prostate cancer
 
A noncomparative randomized phase II study of two dose levels of itraconazole in men with metastatic castration-resistant prostate cancer (mCRPC): A DOD/PCCTC trial. E. S. Antonarakis et al.  J Clin Oncol 29: 2011 (suppl; abstr 4532)
 
At times we rely on the media to let us know when something significant happened at the cancer meetings.  Most of the time, they get it right and breakthroughs get appropriately hyped.  But there was a recent development in prostate cancer which deserves a lot more attention than it has gotten: the use of itraconzole (Sporanox) as a hedgehog inhibitor (HI) in prostate cancer.    Hedgehog inhibition refers to a recent targeted strategy that has met with startling success in patients with advanced basal cell carcinoma and medulloblastoma using vismodegib.  HI is under study in a nearly dozen diseases – including prostate cancer.  Antonarakis and colleagues at Johns Hopkins performed a randomized phase II trial of the antifungal drug itraconazole at 2 dose levels.  The higher dose produced PSA responses > 30% decline in 28% and > 50% decline in 14%.  Serum assays of adrenal androgens were unchanged, suggesting the mechanism was not because of adrenal suppression.  Skin biopsies also demonstrated down regulation of the hedgehog pathway.  For patients who are seeking another strategy to delay cytotoxic therapy with all its attendant challenges, re-tasking itraconazole as an hedgehog inhibitor looks promising indeed.
 
In the coming months, expect to see hedgehog biomarkers that will show us which patients are most likely to respond: patched (PTCH), smoothin (SMO), sonic ligands.  Potentially translational medicine can also mean working from an individual’s cancer to a targeted therapy, a stretch of the traditional notion of testing something in the lab and then giving therapy to everyone.
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Enzalutamide arrives with caveats.
 
Following the terrific introduction of abiraterone (Zytiga) last year for metastatic prostate cancer, the goal posts for hormone sensitivity have again been moved back with the arrival of the new androgen receptor blocker marketed under the name Xtandi.  The new drug gained approval following a prospective, placebo-controlled randomized trial in supposedly hormone refractory patients previously treated with docetaxel chemotherapy: there was a 37% decrease in death rate, and a median survival of 18.4 months compared to 13.6 for placebo. 
 
Unlike its predecessor, bicalutamide (Casodex), severe to life threatening side effects (grader 3-4) were reported in 47% due to asthenia or fatigue, back pain, seizures, diarrhea, arthralgia, hot flush, peripheral edema, musculoskeletal pain, headache, upper respiratory infection, muscular weakness, dizziness, insomnia, lower respiratory infection, spinal cord compression and cauda equina syndrome, hematuria, paresthesia, anxiety, and hypertension.   Some of those may have been associated with disease progression rather than the drug, though by comparison we seldom see any severe toxicity with Casodex.   Thus, while the mechanism may be the same, the collateral issues are not. 
 
Additionally there are a host of drug interaction issues with the hepatic cyclooxygenases CYP2C8, 2C9, 3A4 which requires some advance consideration.
 
Unfortunately the FDA has disappointed us again by labeling the use of the drug after the use of chemotherapy, just as they did for abiraterone.  This runs counter to the basic principle of prostate cancer management, namely to delay the use of cytotoxic therapy for as long as possible.  For our geriatric patients, that principle is even more crucial, and thus, the licensing subjugates the patient’s best interest to an unswerving and blunt, seemingly not well-considered transfer of the criteria for patient participation in a “pivotal” trial to the label. 
 
Mature clinicians know how to take a registration label with a grain of salt when they need to, but unfortunately, the insurance companies walk in lockstep with the label, presumably as a means to avoid paying for new drugs.  Thus, enzalutamide like its predecessor entails writing appeals letters to insurers for pursuing a common sense clinical goal.  Let’s hope the medical directors at the big insurance companies will see this issue clearly and open-mindedly.
 
We also have a few unknowns.  Will it work after abiraterone?  Will it be better tolerated?  Should it supplant Casodex upfront?   These issues will require more study and clinical experience.   But this is one of the examples where a “me-too” drug appears to offer a meaningful step forward for our patients – hooray!
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Beware of xray including mammography if you are carrying a BRCA mutation.
http://group.bmj.com/group/media/latest-news/diagnostic-chest-radiation-before-age-30-may-increase-breast-cancer-risk-in-brca1-2-mutation-carriers

This article in the British Medical Journal is the 2nd paper of its kind showing that BRCA mutation carriers who undergo xrays have an increased risk of being diagnosed with breast cancer.  It's not surprising, because BRCA functions in part as a DNA repair enzyme, and xrays can cause DNA defects that are usually repaired by BRCA and other enzymes.  But for people with BRCA mutations, the repair mechanism has one hand tied behind the back.  There is another carrier state where healthy carriers of the ataxia telangiectasia (AT) gene, also a DNA repair enzyme, have an increase incidence of breast cancer attributable to mammography.  We have known that for a long time.

If you have a life-threatening reason and need to have an xray or a CT scan, then by all means get it done.  But we are talking here about routine screening tests that don't have the same kind of urgency.  In the general population, the risk may be so minimal as to be neglible, but for mutation carriers, the safety margin appears to be absent.  I would say that this includes dental xrays, routine chest xrays, and "casual" xrays done for things like sprained joints.

By comparison, MRI is safe for BRCA carriers, and finds almost all the breast cancers.  Extremely little extra detection of breast cancer comes from the addition a of mammography to MRI, not enough to increase added risk of breast cancer 40-60%.

It is interesting that our European colleagues are way ahead of us on this point.  Therefore, when you discuss this issue with your physicians, be prepared to hear that there is no such recommendation yet in the States, or that your physician has never heard of the issue.  To my knowledge it has not yet even come up in a consensus conference, and thus has not had the hearing it needs.

Finally, the risk that airport scanners pose for people carrying DNA repair enzyme mutations is probably not insignificant.  If you want to avoid getting cancer, I would advise erring on the side of caution and getting frisked instead of going through the airport scanners.  Low dose radiation is oncogenic.
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Michael Castro

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Deja vu from Europe: crizotinib is the new standard of care for ALK positive lung cancer.  Shaw et al ESMO 2012
 
There is a unique kind of lung cancer where a chromosomal rearrangement leads to constitutive activation of ALK that drives proliferation.  In a manner analogous to the use of Gleevec for CML and GIST, crizotinib was approved last year for ALK positive patients after it proved sensationally active in early phase studies. 
 
Now the news from the European cancer meetings that crizotinib is the new standard of care for ALK patient only creates a deja vu impact.  Indeed, we already knew this:  the FDA approved crizotinib based on 2 phase I / II studies that showed astounding efficacy.  The lesson is that when clinically significant benefits are discovered, what we mean by “evidence” need not entail a prospective, doubled blind, placebo-controlled randomized trial.  Actually, we used to know that, too, because much of medical practice came from those remarkable breakthroughs.  For example, there was no need to do randomized trials of penicillin for pneumococcal pneumonia, or thyroid hormone replacement in hypothyroid patients.  And we don’t need a randomized trial to look both ways before crossing the street.
 
Yet this is exactly what was done in ALK positive lung cancer, in spite of the reports that chemotherapy has a 0% response rate published in JCO: 347 patients from 15 centers in Europe were randomized 1:1 to get chemotherapy v. crizotinib.  Not surprisingly, the results were dramatic, even though some responses were observed for chemotherapy.  The primary endpoint of progression-free survival (PFS; independent radiologic review) was 7.7 months (median) in the crizotinib group versus 3.0 months in the chemotherapy group (HR 0.49; 95% CI 0.37–0.64, p<0.0001). The ORR was 65% in patients randomized to crizotinib versus 20% in those randomized to chemotherapy (p<0.0001).
 
Thus, we now have incontrovertible evidence that crizotinib represents the new standard of care for these patients.  But since we already have clinically witnessed one of the most impressive benefits ever observed in lung cancer, might these patients have participated in other trials?  Crizotinib is a giant step forward, but patients eventually progress.  It might have been a better investment of the research dollar to explore trials of post-crizotinib agents for patients, all of whom eventually progress.  
 
Additionally, the ethical issues of consenting patients to the “placebo” arm, in this case chemotherapy, would be difficult for many physicians and I believe impossible for adequately informed patients as well.  The study reported was not mature enough to measure an overall survival difference, but when it is eventually reported in final form, that difference will represent what Dr. Eric Toprol calls the “body bag count” of this population style of science.  While the interests of those with the narrowest concept of what constitutes “evidence” may have been satisfied by this study, the results are unfortunately just old news.  In the genomic era, perhaps we could embrace a more robust concept of evidence.
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TKI therapy for Stage III lung cancer patients: impressive results from the SELECT trial should make the guidelines.
 
SELECT: A multicenter phase II trial of adjuvant erlotinib  in resected EGFR mutation positive NSCLC.  Neal et al. ASCO 2012
 
One of the most pressing questions in thoracic oncology pertains to how we manage EGFR mutation positive patients with non-metastatic disease.  The existing guidelines call for chemo-radiotherapy, however, we have repeatedly learned that there is dramatically superior benefit from using the small molecule EGFR inhibitors, gefitinib and erlotinib in stage IV disease compared to chemotherapy.

This data void was finally filled at the cancer meetings this year with a small multi-institutional trial called SELECT.  Following standard chemo-radiotherapy, patients received 2 years of daily erlotinib with impressive results. The benefits were even more pronounced in patients with the 2 most common EGFR alterations: del19 and L858R.
 
As shown by the survival, benefit of the treatment appears to be cytostatic rather than cytocidal because patients don’t begin to relapse until after the drug is stopped.  This new insight will undoubtedly lead to longer treatment duration in future trials.  Of note, dose adjustment downwards was also required in 39% of patients, indicating that though this is an oral therapy, it requires close supervision.  But at last, it appears we have graduated to a new paradigm in the management of patients with EGFR mt(+) stage III cancer.
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TKI therapy for Stage III Lung Cancer patients: impressive results from the SELECT trial should make the guidelines.
 
SELECT: A multicenter phase II trial of adjuvant erlotinib  in resected EGFR mutation positive NSCLC.  Neal et al. ASCO 2012
 
One of the most pressing questions in thoracic oncology pertains to how we manage EGFR mutation positive patients with non-metastatic disease.  The existing guidelines call for chemo-radiotherapy, however, we have repeatedly learned that there is dramatically superior benefit from using the small molecule EGFR inhibitors, gefitinib and erlotinib in stage IV disease compared to chemotherapy.

This data void was finally filled at the cancer meetings this year with a small multi-institutional trial called SELECT.  Following standard chemo-radiotherapy, patients received 2 years of daily erlotinib with impressive results of a 94% disease free survival. The benefits were even more pronounced in patients with the 2 most common EGFR alterations: del19 and L858R.
 
Interestingly, benefit of the treatment appears to be cytostatic rather than cytocidal because patients don’t begin to relapse until after the drug is stopped.  This new insight will undoubtedly lead to longer treatment duration in the future.  Dose adjustment was also required in 39% of patients, indicating that though this is an oral therapy, it requires close supervision.  But at last, it appears we have graduated to a new paradigm in the management of patients with EGFR mt(+) stage III cancer.
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PomX increases PSA doubling time
 
A phase II study of pomegranate extract for men with rising prostate-specific antigen following primary therapy. Paller C et al.  J Clin Oncol 29: 2011 (suppl; abstr 4522)
 
The group from UCLA and Johns Hopkins reported follow-up data to a study that was first reported at the chemotherapy meetings in NY last November.  The performed a multi-institutional double-blind trial of pomegranate extract at 2 dose levels and measured the change in baseline PSA doubling time (PSADT) in 104 patients with a median age of 74 and Gleason score of 7.   The median PSADT increased from 11.9 months to 18.5 months.  The lower dose (1 g/day) worked as well as the higher dose (3 g/d).  PSA levels declined in 13%, and rose by 200% among 43% of patients who developed no new metastases.  No change was seen in serum testosterone levels, and no clinically significant toxicities occurred, though 8% of patients reported mild diarrhea.
 
This report adds to a growing literature about the anti-cancer properties of a food substance.  Though the mechanism remains to be elucidated, many food-related chemicals appear to reverse the methylation status that inactivates tumor suppressor genes.
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Is your KRAS result correct? http://jcp.bmj.com/content/65/10/940.abstract?ct=ct
For patients with colorectal cancer, KRAS mutations determine resistance to EGFR antibody drugs.  Patients without mutations have a good chance to respond to those drugs.   But if you can't get a benefit, there's no sense putting up with the side effect of rash.  This new paper from Italy shows that the site of the biopsy is important: when the primary site (i.e. the GI tract) is used instead of the metastatic site (i.e. such as the liver), there is a false negative of about 1/6.  This would lead to use of an EGFR blocking antibody that has little to no chance to be of any value.  False negatives also occur when the tumor cellularity in the specimen is less than 30%.

It's not just that an ineffective drug will be given in those cases, but there are now new agents in development for blocking KRAS mutations, such as selumetinib and ERK inhibitors.  If you have a KRAS mutation, you definitely want to be looking into those possibilities.  KRAS drives tumor proliferation and blocks the tumor cell's ability to die.  It is an important mechanism of drug resistance.  BTW, there is an interesting literature that the anticholesterol drug simvastatin is an effective KRAS blocking agent, but no one spends a dime on generic drugs, and so unfortunately this potential diamond in the rough will remain in obscurity.

It is also possible that the tumor's KRAS status could change over time.  When in doubt consider re-biopsy.  A little extra scrupling about KRAS could make a difference.
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Hype without substance: combination endocrine therapy in breast cancer: anastrolozole plus fulvestrant. http://www.nejm.org/doi/full/10.1056/NEJMoa1201622

When they're useful, phase 3 trials employ the existing standard of care as a control arm, thereby allowing a positive result to be interpreted clearly for patient management.  But in the study by Mehta and colleagues testing anastrozole-fulvestrant v. anastrozole alone, only 41% crossed over from anastrozole to receive an antiquated low dose of fulvestrant, representing a serious error in study design.  After all, the goal is to keep patients off chemotherapy for as long as possible, and using any number of hormonal therapies to achieve that end.  Without a sequential control arm, a minimum of at least 2 anti-estrogen therapies, the study is of no relevance to clinical practice.  While the authors tell us the sequentially-treated minority of patients fared worse, they don't show the data (an un-forgiveable omission...!).  Moreover, the survival curves show that at least 45% of the patients on the combination arm derived no benefit.  For the remaining 55%, the survival curves don't begin to separate for a year, suggesting that there is an awful lot of sore butts from bilateral intramuscular injections for a long time who got no benefit from combined therapy.  Arguably this group could have gotten fulvestrant after anastrolzole and had just as large an increment, and many healthcare dollars would be saved in the process. 

What about that only 40% of the patients in the study ever received tamoxifen, and in that group who got tamoxifen, there was no benefit from the combination of the 2 drugs.  Also a study published in J. Clin Oncol called the FACT trial this year, 70% of the patients had received tamoxifen before and that trial could not demonstrate any benefit for the combination. 

Therefore the new study is unconvincing, and taken collectively suggests that getting a SERM like tamoxifen or faslodex at some point in the course of treatment is important, but do not convince us that the combination is better.

There are other distressing things about the way the data were presented or not presented.  For example, we are not told whether the treatment arms were evenly balanced according to the degree of expression of estrogen receptor, progesterone receptor, and Ki-67, even though such a discrepancy could easily explain a  difference in outcome.

Most surprisingly, the authors suggest this should be a new standard of care despite the fact that the biggest discovery in a decade has been reported this year in breast cancer using aromatase inhibitors plus everolimus or tamoxifen plus everolimus.  The mTOR inhibitor, everolimus, reverses drug resistance and increases the duration of benefit by 2.5x.  By comparison, the proposed use of anastrozole and fulvestrant makes no sense.

I hope we are not going to embark on a large expensive adjuvant trial of this approach, but I fear the machine of industry may be at work to make this happen.  If there are people who would benefit from combination therapy, we should try to find out who they are, and get away from the blunt approach of giving everyone the needlessly expensive one-sized fits all therapy.  It is high time to evolve.
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