Reporters:
Larry H. Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN
Word Cloud By Danielle Smolyar
DNA pioneer James Watson takes aim at “Cancer establishments”
By Sharon Begley
| Sharon Begley, the senior health & science correspondent at Reuters, was the science editor and the science columnist at Newsweek from 2007 to April 2011, and a contributing writer at the magazine and its website, The Daily Beast, until December 2011. From 2002 to 2007, she was the science columnist at The Wall Street Journal, and previous to that the science editor at Newsweek. She is the co-author (with Richard J. Davidson) of the 2012 book The Emotional Life of Your Brain, the author of the 2007 book Train Your Mind, Change Your Brain, and the co-author (with Jeffrey Schwartz) of the 2002 book The Mind and the Brain. She is the recipient of numerous awards for her writing, including an honorary degree from the University of North Carolina for communicating science to the public, and the Public Understanding of Science Award from the San Francisco Exploratorium. She has spoken before many audiences on the topics of science writing, neuroplasticity, and science literacy, including at Yale University (her alma mater), the Society for Neuroscience, the American Association for the Advancement of Science, and the National Academy of Sciences.Follow me on Twitter: https://twitter.com/sxbegle for breaking science news, not what I’m having for breakfast. |
- On the $100 million U.S. project to determine the DNA changes that drive nine forms of cancer: It is “not likely to produce the truly breakthrough drugs that we now so desperately need,” Watson argued. On the idea that antioxidants such as those in colorful berries fight cancer: “The time has come to seriously ask whether antioxidant use much more likely causes than prevents cancer.”
- The main reason drugs that target genetic glitches are not cures is that cancer cells have a work-around. If one biochemical pathway to growth and proliferation is blocked by a drug such as AstraZeneca‘s Iressa or Genentech’s Tarceva for non-small-cell lung cancer, said cancer biologist Robert Weinberg of MIT, the cancer cells activate a different, equally effective pathway.
- That is why Watson advocates a different approach: targeting features that all cancer cells, especially those in metastatic cancers, have in common.
- One such commonality is oxygen radicals. Those forms of oxygen rip apart other components of cells, such as DNA. That is why antioxidants, which have become near-ubiquitous additives in grocery foods from snack bars to soda, are thought to be healthful: they mop up damaging oxygen radicals.
- That simple picture becomes more complicated, however, once cancer is present. Radiation therapy and many chemotherapies kill cancer cells by generating oxygen radicals, which trigger cell suicide. If a cancer patient is binging on berries and other antioxidants, it can actually keep therapies from working, Watson proposed.
- “Everyone thought antioxidants were great,” he said. “But I’m saying they can prevent us from killing cancer cells.”
- One elusive but promising target, Watson said, is a protein in cells called Myc. It controls more than 1,000 other molecules inside cells, including many involved in cancer. Studies suggest that turning off Myc causes cancer cells to self-destruct in a process called apoptosis.
- “The notion that targeting Myc will cure cancer has been around for a long time,” said cancer biologist Hans-Guido Wendel of Sloan-Kettering. “Blocking production of Myc is an interesting line of investigation. I think there’s promise in that.”
- Targeting Myc, however, has been a backwater of drug development. “Personalized medicine” that targets a patient’s specific cancer-causing mutation attracts the lion’s share of research dollars.
- “The biggest obstacle” to a true war against cancer, Watson wrote, may be “the inherently conservative nature of today’s cancer research establishments.” As long as that’s so, “curing cancer will always be 10 or 20 years away.”(Reporting by Sharon Begley; Editing by Jilian Mincer and Peter Cooney)
SOURCE:
http://in.reuters.com/article/2013/01/09/usa-cancer-watson-idINDEE90804520130109
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Very interesting ideas from so prominent scientist.
But the main paradigm question is: “Is Cancer Cell a cause of Cancer?”
If “yes”, it mean this is a right direction and we can develop Myc drugs, or replace them by other tools (according to which industry have more funding potential – same “attracts the lion’s share of research dollars”).
But if “no” this mean we are searching not for right things. This mean that any effort oriented on Cancer Cell (in diagnostic or treatment) is wasting of time! This alternative paradigm position have absolutely no funding!
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Please review the following to find an answer ot your question, above:
“The Molecular pathology of Breast Cancer Progression”
http://pharmaceuticalintelligence.com/2013/01/10/the-molecular-pathology-of-breast-cancer-progression/
Great topic Larry
sorry if my previous response was lost as it was about a page long. It is somewhere out there. To summarize, I applaud both Watson and Weinstein (who made the chief discovery of a set of multiple genetic events that can fully transform human cells into the malignant state) for their brave take on current state of affairs. As I mentioned in a previous comment to one of your posts the role of antioxidants in oncogenesis and tumor progression is very confusing. For instance clinical trials involving lung cancer risk and vitamin A intake were not conclusive at all, and later found that smokers actually had increased lung cancer risk if taking vitA supplementation. Same confusion with VitE/selenium and prostate cancer trials. In addition I remember back in the 90s when big pharmas were talking about developing farnesyltransferase inhibitors (the enzyme that puts the modification on ras) as well as myc inhibitors as a sliver bullet for cancer therapy but I have not heard much else. Interesting. And as far as personlized medicine, yes personalized medicine does have a role to play and can be very effective but remember we are only talking about maybe 10% of cases for a tumor type. Kudos to both Watson and Weinstein for stating we really need to delve into tumor biology to determine functional pathways (like metabolism) which are a common feature of the malignant state ( also see my posting on differentiation therapy).
Great post Larry, enjoyed reading the post and the comments.
I agree with Dr. Williams on this. Several clinical trials also tried to evaluate the benefits of vitamins (A,E etc) in decreasing breast cancer progression or preventing its recurrence. Results of the these clinical trials were also somewhat confusing and unfortunately, no clear massage was given to the patients.
I would like to add something regarding this comment and I quote “the main reason drugs that target genetic glitches are not cures is that cancer cells have a work-around. If one biochemical pathway to growth and proliferation is blocked by a drug such as AstraZeneca‘s Iressa or Genentech’s Tarceva for non-small-cell lung cancer, said cancer biologist Robert Weinberg of MIT, the cancer cells activate a different, equally effective pathway”
I think this is why some researching are aiming to find a drug that targets a common denominator of multiple pathways rather that “just” a specific pathway as many cancer cells activate a different equal pathway.
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The progress made in targeting specific genetic pathways has been impressive, but the issue of physical delivery of the drug to the target site appears to be a key to the success of these new treatments.
While cancer cells do develop “work-around” biochemical responses, and tumor heterogeneity factors frustrate specific targeting, the consistency in physiological construct makes it possible to concentrate drugs based on rationally designed delivery systems.
The work by Dr. Mauro Ferrari has provided significant progress in this area and the improvements his group has achieved in both improved efficacy and reduced toxicity have been impressive thus far.
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