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'Missing link' to cancer is found.

'Missing link' to cancer is found

A scientist described last week what he calls the first product of a cancer gene known to bind with human DNA and directly control the activity of other cellular genes. Researchers found the gene product, a protein, by focusing on one of its many targets, a gene involved in regulating zinc metabolism. But its real significance, says Michael Karin, who led the team discovering it, is that it "was the missing link in the whole concept of how cancer occurs."

For years, scientists have believed cancer occurs when the normal processes regulating cell growth somehow get out of control. And there has been evidence for aberrant regulation in every step of the cellular growth-control process except the last one, Karin says. Researchers have seen aberrations in the production of hormonal growth factors that bind to cells, in the activity of the cell-surface receptors for those growth factors and in the enzymes that translate the receptors' activity into chemical messages that control cell growth. Missing was evidence that proteins carrying these chemical messages not only would bind to the cell's DNA but also would trigger the expression of genes in the cell nucleus. And that's what the University of California at San Diego team has found. Says Karin, "It's like finding the Rosetta stone" for cancer.

The newly identified cancer-gene-derived protein, triggered by an animal virus, resembles "activator protein 1," or AP-1, present in all normal cells. As a "transcription factor," AP-1 is able to switch on the transcription machinery -- which copies DNA into RNA -- of genes in the cell nucleus, Karin says. And at least by function, he says, "we cannot distinguish between AP-1 and its [cancer-gene-derived] homolog."

The cancer gene's protein appears to cause cancer by turning on a process that ultimately leads to cell division. But because the virus carrying the cancer gene overproduces this protein, the cellular proliferation process never shuts off -- and a cancer is born. Ordinarily, regulation of AP-1 in normal cells is tightly controlled. When triggered into action it does its job and then stops. But certain cancers -- most notably lung cancer -- contain an excess of AP-1. Karin says it appears the AP-1 excess operates in precisely the same way as the massively produced cancer-gene homolog -- triggering runaway cell proliferation and the cancer. Karin hopes that by studying the genes targeted by AP-1 -- whether it's produced at normal levels or at high levels -- he can gain a better understanding of the mechanisms of cancer and clues to its undoing.
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Author:Raloff, Janet
Publication:Science News
Date:Jun 18, 1988
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