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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.

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Credit: Tan Ince (top), Sam Ogden/Whitehead Institute (bottom)

Tagged: Biomedicine, cancer, stem cells, tumor, embryo

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