The Chinese Solar Machine Layer by Layer Fire in the Library The Mystery Behind Anesthesia
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TR: If cancer cells are similar to normal embryonic cells, is it surprising that we don't get cancer more often or earlier?
RW: It says, rather, that cancer cells are not as clever as we think they are. Rather than having to cobble together complex behavioral problems, they simply resort opportunistically to resurrecting behaviors which are normally suppressed in adult tissue, and therefore do not represent an imminent threat to the organism because they're kept under tight control. (There are multiple mechanisms implanted in our cells and tissues that impede the formation of tumors.)
This scenario I've just depicted is very heartening for us because if one looks at the biology of metastatic cells, it seems to be so complex as to be bewildering beyond anyone's ability to understand it, simply because there are so many different genes and proteins involved. However, if one is now able to trace these behaviors to a small number of central regulators, each of which can act by modulating the expression of a whole cohort of responder genes, now one has greatly simplified the problem, because now one can focus one's attentions on two or three distinct central regulators that choreograph the traits of high-grade malignancy.
TR: How has our understanding of cancer changed during your career?
RW: In the mid 1970s, we knew nothing about why cancer cells misbehaved. We knew they did misbehave, but they were a black box. Over the next quarter century, there was an enormous avalanche of information that came out that described the fact that many but perhaps not all the traits of cancer cells and tumors could be ascribed to damaged genes that reside within the cancer cells. Prior to 1975, that was a total speculation. So there's been a radical about-face in terms of that. Now cancer is no longer a mystery in terms of how it arises.
TR: What big questions remain?
RW: What we still don't really understand is why certain people get cancer and other people don't. We understand that people get lung cancer because they smoke. But we don't really understand why they get breast or prostate cancer--yet. But I think that will emerge with increasing clarity over the next decade. Still, we know quite a bit about why breast-cancer cells misbehave, while at the same time being able to point to the causative factors of lifestyle and family history that dictate their susceptibility to developing the disease.
TR: When is there going to be a cure for cancer?
RW: If you look at the death rates for cancer in this country, they've been going down for most but not all kinds of cancer. There's not going to be a single, dramatic cure. Instead, there will be a series of cures that will be developed over the years that will progressively lower the death rate. It's going to be incremental gains. There may be certain dramatic battles that are won--certain kinds of cancers will be converted from a life-threatening to a chronic disease.
In the long run, the biggest reductions in cancer mortality will actually come from prevention, not treatment. So one can probably halve, maybe even decrease by two-thirds, one's risk of getting cancer by not smoking, by not living with smokers, by staying slim, by having a diet which is high in vegetables and low in red meats, by getting exercise, and maybe in the future by taking different kinds of vitamins. It's still a little bit sketchy as to which ones. The risk of dying from cancer, which is now about one in five, may go down to one in ten, or one in fifteen. Could be.
a few cancers are composed of diploid cells, but most have an abnormal triploidy as well as chromosome malarrangement;hance, to regress when injected into an embyro, and revert to normal seems moot.how do we know that the cancer cells did not take hold and died? were the cancer cell labled with a tag, to determine that they actually reverted to normal.
regardless, as crazy as it sounds, maybe the reseach has merit. there are many lessons in the history of science where cockeyed ideas eventually were proven true. think, the cloning of dolly, the dogma was that it couldn't be done.
to me one of the greatest hinderance to the progress of science is the hiarchical funding (which is blinded by conventional wisdom) of research. Those with the creative ideas never get a chance to explore their "crazy" ideas.
ron hansing
Funding yes, was it Otto Warburg who first observed the similar growth rates of an embryo and a tumor, and that they both appeared to run on glycolysis? How very long ago was that. How I wish there was no church lady in the laboratory or fuding considerations. But as you say, there is a heirarchy to deal with too. Politics of one type or another, while 580,000 die per year and a similar number maimed by today's "treatments".
Manufacturing in the United States is in trouble. That's bad news not just for the country's economy but for the future of innovation.
ajimenez
14 Comments
Embryological Cancer Cells
I believe that a single cure is possible. If the cancer cell reverts to an earlier embryological stage then there is a very good possibility that the cell's program could be "fast forwarded" to an adult phenotype. Perhaps something innocuous like connective tissue.
I have had these ideas ever since the '70's when I heard about a woman biologist who put cancer cells into a developing embryo and then noticed that the cancerous state disappeared. For more details on this please see my blog: http://ortholex.blogspot.com
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prime3end
13 Comments
Re: Embryological Cancer Cells
Its completely in line with Weinberg and others' work, many others. Telomerase switches 217 genes to cancer mode, turning on 76 genes associated with growth (Elizabeth Blackburn co discoverer of telomerase). It allows cells to overcome the hayflick limit, so achieving replicative immortality. Telomerase also turns on glycolysis in melanoma (and probably other cancers) per Mohammed Kashani-Sabet UCSF and Blackburn et al. He observed some normalization of melanoma cells when telomerase was inhibited, also cell death. Glycolysis is of course cancers monstrous energy source. When Evangelos Mikelakis at U of Alberta used sodium dichloroacetate to treat human breast brain and lung cancer in rats, he saw 70% tumor reduction in 3 weeks. He was stopping glycolysis. Now imagine effective telomerase inhibition with an additional direct attack on glycolysis. Close monitoring would be required to limit tumor lysis syndrome,,, which is too many cells dying to fast for the body to purge/process them. Feel free to contact me for links to the work I cite if you are a researcher or doc. I'm not selling anything. Also in todays news, several cancer causing viruses were studied and it was found that they actively hijack telomerase production to magnify their own numbers, providing growth in otherwise senescent cells. The paper continues that this growth allows for further mutations in ,, well perhaps in Weinbergs other two genes he uses to cause cancer in "many human cell types", a tumor suppressor gene and an oncogene. Telomerase is the first step in tumorogenisis. A cancer and an embryo are more like each other, than like a normal cell. prime3end@yahoo.com www.geocities.com/prime3end
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