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Chemotalk NewsletterChemotalk Newsletter, Vol. 56: December 1, 2012 At last, no more political ads! How long do you think we have before it starts all over again? And on that note, some REALLY positive news .... (Okay, it's a start. A good one:) SANOFI HALVES PRICE OF CANCER DRUG ZALTRAP AFTER SLOAN-KETTERING REJECTION By Andrew Pollack In an unusual move a big drug company said that it would effectively cut in half the price of a new cancer drug after a leading cancer center said it would not use the drug because it was too expensive. The move -- announced by Sanofi for the COLON CANCER drug Zaltrap -- could be a sign of resistance to the unfettered increase in the prices of cancer drugs, some of which cost more than $100,000 a year and increase survival by a few month at best. Zaltrap came to market at a price of about $11,000 a month. Soon after, Memorial loan-Kettering Cancer Center in New York decided not to use the drug, saying it was twice a expensive but no more effective than a similar medicine, Avastin from Genentech. Both drugs improved median survival by 1.4 months, doctors there said. "Ignoring the cost of care is no longer tenable," according to three S-K doctors who posted their opinion in a recent Op-Ed piece. "Soaring spending has presented the medical community with a new obligation. When choosing treatments for patients, we have to consider the financial strains they may cause alongside the benefits they may deliver." Sanofi executives argued that the price they had set was very similar to that of Avastin. "The intent was not to charge a premium," Christopher A Viehbacher, the chief executive of Sanofi, said in an interview. Sloan-Kettering, he said, was basing the price comparison on a dose of Avastin that was half the dose Sanofi used in its own comparison. Sanofi ultimately backed down, saying "We believe that Zaltrap is priced competitively as used in real-world situations," it said in a statement. "However, we recognize that there was some market resistance to the perceived relative price of Zaltrap in the U.S. -- especially in light of low awareness of Zaltrap in the U.S. market. As such, we are taking immediate action across the U.S. oncology community to reduce the net cost of Zaltrap." The move was first reported in The Cancer Letter, a newsletter about cancer issues. Sanofi said it would not change the official price of Zaltrap but would offer discounts of about 50%. Zaltrap, which is given intravenously is not bought directly by patients but I sold to doctors or hospitals, which administer it. The cost is then reimbursed by Medicare or private insurers. Patients could be liable for a co-payment. Dr. Leonard B. Saltz, chief of gastrointestinal oncology at Sloan-Kettering, said Sanofi's offer of discounts "doesn't really address the problem from our perspective" because Medicare reimbursement an patient co-payments would still be based on the higher list price at least for several more months. Also, he said, the discounts could give doctor and hospital an incentive to use Zaltrap because they could profit from the difference between the discounted price they pay for the drug and the higher price at which they are reimbursed by insurers. Dr Saltz said even at the lower price he did not foresee Sloan-Kettering doctors using Zaltrap because it was no better than Avastin and might be more toxic. Dr Saltz is now a consultant at Genentech and has been one to Sanofi. Zaltrap, developed by Sanofi and Regeneron Pharmaceuticals a biotechnology company in Tarrytown, N.Y, was approved by the Food and Drug Administration in August for use as a second-line treatment for COLORECTAL CANCER, meaning after an initial regimen had stopped working. Like Avastin, Zaltrap ipedes the formation of bloos vessels that nourish cancer cells. Dr. Peter B. Bach, director of the Center for Health Policy and Outcomes at Sloan-Kettering, said the price of Zaltrap reflected a bigger problem -- that over all there was little relation between drug prices and the value they provided. "Normal markets wouldn't behave like this," he said. "You couldn't introduce something twice as expensive and no better an still sell it." Dr. Lee Newcomer senior vice president for oncology at United Healthcare, said it was the first time he could recall a company cutting the price of a cancer drug so much. "It was the first time physician have stood up and said 'Enough is enough,'" he said. "And I think that was a watershed moment." * * * DRUG APPEARS PROMISING FOR HEAD AND NECK CANCER Australian biotech startup MiReven says it has produced encouraging preclinical results using a microRNA substance in conjunction with a Roche/Genentech drug to treat HEAD AND NECK CANCER. Researchers from the Western Australian Institute for Medical Research pursued the work regarding miR-7's cancer-fighting ability. (MiReven's core technology is licensed from initial work conducted at the institute.) They explored two options: How well miR-7 could restrict head and neck cancer growth in vivo, and the effectiveness of doing the same thing, in vitro, by combining miR-7 with the Roche/Genentech drug erlotinib (Tarceva). Erlotinib inhibits epidermal growth factor (EGF), which is an effective treatment in between 20% and 30% of patients with head and neck cancer. The idea is that miR-7 can knock out the EGF receptor, an essential element that sustains cancer and can make it resistant to both CHEMOTHERAPY and radiation. Could the combined treatment be even more powerful? The answer, so far, appears to be yes. MiReven, which launched in 2010, said that miR-7 on its own appeared to shut down aspects of EGF. But the combined treatment made miR-7 even more potent, the scientists said. It is a positive initial result, but broader animal studies are needed before the treatment can be tested in human trials. It will be some time before this treatment reaches human patients, assuming subsequent testing bears out its initial promise. MiReven is counting on success. Company chairman Stephen Thompson said in a statement that once a number of studies now under way are complete, MiReven will seek a corporate partner to advance miR-7 into clinical trials. * * * From the Op-Ed pages of The New York Times, written by a primary care internist and assistant professor at the Yale School of Medicine, the following article lifts the curtain a little for a look into the world of medical billing: A SHORTCUT TO WASTED TIME By Leora Horwitz A few years ago, we doctors kept handwritten charts about patients Back then, it sometimes seemed like we spent half our time walking around looking for misplaced charts, and the other half trying to decipher the handwriting when we found them. The upside was that if I did have the chart in front of me, and I saw that someone had taken the trouble to write something down I believed it. Unfortunately, this is no longer the case. The advent of electronic medical records has been a boon to patient safety and physician efficiency in many ways. But it has also brought with it a slew of "timesaving" tricks that have had some unintended consequences. These tricks make it so easy for doctors to document the results of standard exams and conversations with patients that it appears more and more of them are being documented without ever having happened in the first place. For instance, doctor used to have to fill out a checklist for every step in a physical exam. Now, they can click one button that automatically places a comprehensive normal physical exam in the record. Another click bring up a normal review of systems -- the series of screening question we ask patients about anything from nasal congestion to constipation. Of course you shouldn't click those buttons unless you have done the work. And I have many compulsively honest colleagues who wouldn't dream of doing so. But physicians are not saints. Hospitals received $1 billion more from Medicare in 2010 than they did in 2005. They say this is largely because electronic medical records have made it easier for doctors to document and be reimbursed for the real work that they do. That's probably true, to an extent. But I bet a lot of doctors have succumbed to the temptation of the click. Medicare thinks so too. This fall, the attorney general and secretary of health and human services warned the five major hospital associations that this kind of abuse would not be tolerated. And then there are the evil twins, copy and paste. I've seen "patient is on day two of antibiotics" appear for five day in a row on one chart. Worse, I've seen my own assessments of a a patient's health appear in another doctor' notes. A 2009 study found that 90% of physicians reported copying and pasting when writing daily notes. In short reading the electronic chart has become a game of looking or a small needle of new information in a haystack of falsely comprehensive documentation and outdated copied text. Why do we doctor do this to ourselves? Largely, it turn out, for the same reason most people do most things: money. Doctors are paid not by how much time they spend with patients, how well they listen or how hard they think about what could be wrong, but by how much they write down. And the rules for what we have to write are Byzantine: Medicare's explanation takes 87 pages To receive the highest level of payment for an office visit, I have to document several aspects of the main problem screening questions about at least 10 organ systems, something about the patient's family and/or social history, and/or a lengthy physical exam. In addition, I have to demonstrate that my medical decision making was very complicated, considering the number of possible diagnoses and treatments, the complexity of the data and/or the patient' risk of serious complication. That type of visit is supposed to take about 40 minutes. Last week, I spent 40 minutes with a patient who had just placed her mother into hospice care. My patient was distraught, not sleeping, not eating. I gave her some advice, but mostly I jut listened. By the end of our visit, she was feeling much better. But I wouldn't be able to bill much for that visit based a review of organ systems or perform a physical exam. What the payment system tells me to do is to cut her off after 10 minutes, listen to her heart and lungs and give her a sleeping pill. Which doctor visit would you prefer? Of course, I would never go back to the bad old days of lost charts, illegible writing, manual prescription refills and forgotten information. Electronic medical records help us avoid dangerous drug interactions and medical ordering errors, remind us to provide preventive care and allow us to view data as trends over time. Even copy and paste have legitimate uses. But physicians need to be better stewards of our records so they remain useful, regardless of skewed incentives and new technology. And as a nation, we should question whether paying physicians by documentation -- instead of by time spent on quality patient care -- is such a great idea after all. * * * NEW DRUG CREDITED WITH SLOWING PANCREATIC CANCER TUMOR GROWTH Swedish drug developer Kancera says it has slowed the growth of PANCREATIC CANCER tumors in preclinical animal trials with its first-generation PFKFB3 inhibitors. The drug initially failed to work in an animal study involving human COLON CANCER, according to the company. By blocking PFKFB3, the idea is to reduce the metabolism of the cancer tumors and starve its energy/food supply. PFKFB3 is believed to support cancer growth because it enables production of glucose, which cancer craves. Kancera claims that the drug generated a 20% reduction in pancreatic cancer tumor growth versus placebo treatment. That may not sound like a lot, but as the company notes, patients diagnosed with pancreatic cancer have a less than 2% survival rate 5 years after the diagnosis. And so Kancera insists that the initial promise PFKFB inhibitors show in reducing pancreatic cancer growth is license to proceed. "That PFKFB inhibitors alone can reduce the growth of pancreatic cancer is very encouraging," CEO Thomas Olin said in a statement. Kancera's initial results are encouraging but they're a long way from human trials. Coming next will be a bid to improve the drug properties of the company's PFKFB inhibitors and test how well they work to combat tumor growth combined with standard pancreatic cancer therapy. Kancera isn't the only company targeting PFKFB3, whose full name is 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3. Advanced Cancer Therapeutics is developing a possible BRAIN CANCER treatment with the same enzyme target in mind. * * * FDA APPROVES RHEUMATOIR ARTHRITIS PILL Pfizer Inc. has received approval from the U.S. Food and Drug Administration (FDA) for XELJANZ® (tofacitinib citrate) 5 mg twice daily for the treatment of adults with moderately to severely active RHEUMATOID ARTHRITIS who have had an inadequate response or intolerance to methotrexate. XELJANZ may be used as monotherapy or in combination with methotrexate or other non-biologic disease-modifying antirheumatic drugs (DMARDs). XELJANZ should not be used in combination with biologic DMARDs or with potent immunosuppressives, such as azathioprine and cyclosporine. XELJANZ (ZEL'jans') is the first approved RA treatment in a new class of medicines known as Janus kinase (JAK) inhibitors and the first new oral DMARD approved for RA in more than 10 years. * * * SCIENTISTS CRACK GENETIC CODE FOR RARE CHILDHOOD LEUKEMIA VARIATION Scientists believe they've cracked the code to a rare variation of childhood LEUKEMIA, and the key involves an abnormal gene. Researchers at St. Jude's Children's Research Hospital and Washington University jointly pursued the research, which is highlighted in detail in the journal Cancer Cell. And their finding could lead to better diagnostic tools and new treatments for patients with ACUTE MEGAKARYOBLASTIC LEUKEMIA (AMKL), which affects 10% of children with PEDIATRIC ACUTE MYELOID LEUKEMIA. The key turns out to be the CBFA2T3-GLIS2 protein, a weird fusion of what is normally a blood protein and a protein typically produced in kidneys. Researchers determined in the lab that the CBFA2T3-GLIS2 fusion gene is key because it turns on other genes that propel immature blood cells to keep dividing even as normal cells pass on, something that is channeled directly into the emergence of leukemia. What's more, treatments seem to be at a high risk of failure for patients found to have the CBFA2T3-GLIS2 fusion gene, according to the research team. But checking long-term survival records of 40 AMKL patients globally, they found that just 28% of patients who had the gene fusion survived long-term. For patients without the gene, that number jumped to 42%. Corresponding author Dr. James Downing, scientific director at St. Jude, said in a statement that the finding should help boost both diagnostic testing and more targeted, therapeutic treatments. That may be true in the long term, but the research is years away from fruition. What it does, however, is open the door to the development of more targeted treatments. In the future, it could also enable earlier diagnosis, and a more rapid treatment might help increase survival times. St. Jude and Washington University are in the midst of a three-year collaboration known as the Pediatric Cancer Genome Project, where they are focusing on sequencing both normal and cancer genomes from 600 children and teens who have aggressive and rare cancers. * * * See you next year .. * * * And if you have any thoughts of how this newsletter could be improved, please email me directly, at Elaine@elainejesmer.com. Elaine Jesmer
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