Oncogenes are genes that cause cancer.
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Oncogenes are genes that cause cancer. They were first found in viruses, but their evolutionary history implies that normal vertebrate cells have genes whose abnormal expression can lead to cancerous growth, as this article from Scientific American explains. Oncogenes Can the cancer cell be understood? Since no one can yet explain how a normal cell controls its growth, it may seem foolhardy to think the abnormal rules governing the growth of a cancer cell can be deciphered. Yet the history of biology records many instances in which the study of abnormalities has illuminated normal life processes. Recent developments in cancer research have added a dramatic new example. For the first time investigators have perceived the dim outline of events that can induce cancerous growth. Enzymes that catalyze those events have been identified, and so have the genes specifying the structure of the enzymes. These advances have come from the study of viruses that induce tumors. Recent years have seen an enthusiastic search for viruses that cause cancer in human beings. The search has been largely unsuccessful, leading many informed observers to doubt that viruses will ever prove to be a major cause of human cancer. Some viruses do induce tumors in other animals, however, and investigators have been studying these tumor viruses, attempting to define fundamental derangements of the cell that are responsible for cancerous growth. That quest has struck gold. Although the genes implicated in the development of cancer were first observed in work with viruses, they are not native to the viruses. Indeed, it has turned out that the genes are not even peculiar to cancer cells. They are present and functioning in normal cells as well, and they may be as necessary for the life of the normal cell as they appear to be for the unrestrained growth of a cancer. A final common pathway by which all tumors arise may be part of the genetic dowry of every living cell.
Experiments by Hartmut Beug and Thomas Graf of the Max Planck Institute for Virus Research in Tübingen showed, however, that the effects of the src protein can be detected even in cells from which the nucleus has been removed. It came as no surprise, then, when several workers found that little if any of the pp60v-src in transformed cells is in the nucleus. Most of the protein is at the other extreme of the cell: it is bound to the plasma membrane, the thin film that encloses the cell and mediates its interactions with the outside world. Many cell biologists have argued that the control of cell growth may originate at the plasma membrane and its associated structures. Inspection of the plasma membrane of cells transformed by src has provided the first correlation between the action of pp60v-src on a specific cellular protein and one of the typical changes in structure and function seen in cancer cells. By means of specialized techniques of photomicroscopy Larry R. Rohrschneider of the Fred Hutchinson Cancer Research Center in Seattle was able to demonstrate that pp60v-src is concentrated in adhesion plaques: regions of the membrane that adhere to solid surfaces. In cancer cells the adhesion plaques are dismantled; the resulting decrease in cell adhesion may contribute to the ease with which most cancer cells break away from their tissue of origin and metastasize to other sites. Rohrschneider's findings suggested that pp60v-src might dismantle adhesion plaques by phosphorylating one of their component proteins, or perhaps several of those proteins. Pursuing that suggestion, Sefton and S. J. Singer of the University of California at San Diego showed that pp60v-src phosphorylates a tyrosine unit in vinculin, a protein that is a constituent of normal adhesion plaques and becomes dispersed throughout the cell following transformation by src. It seems reasonable to suggest that the phosphorylation of vinculin precipitates the dismantling of adhesion plaques, but the importance of such events in the unruly behavior of cancer cells has yet to be established.
Yet it is clearly possible that there is only one large family of cellular oncogenes. If that is so, the study of retroviruses and the procedures developed by Weinberg and Cooper should eventually begin to draw common samples from that single pool. A Final Common Pathway Normal cells may bear the seeds of their own destruction in the form of cancer genes. The activities of these genes may represent the final common pathway by which many carcinogens act. Cancer genes may be not unwanted guests but essential constituents of the cell's genetic apparatus, betraying the cell only when their structure or control is disturbed by carcinogens. At least some of these genes may have appeared in retroviruses, where they are exposed to easy identification, manipulation and characterization. What has been learned from oncogenes represents the first peep behind the curtain that for so long has obscured the mechanisms of cancer. In one respect the first look is unnerving, because the chemical mechanisms that seem to drive the cancer cell astray are not different in kind from mechanisms at work in the normal cell. This suggests that the design of rational therapeutic strategies may remain almost as vexing as it is today. It will be of no use to invent means for impeding the activities responsible for cancerous growth if the same activities are also required for the survival of normal cells. However the sage of oncogenes concludes, it presents some lessons for everyone concerned with cancer research. The study of viruses far removed from human concerns has brought to light powerful tools for the study of human disease. Tumor virology has survived its failure to find abundant viral agents of human cancer. The issue now is not whether viruses cause human tumors (as perhaps they may, on occasion) but rather how much can be learned from tumor virology about the mechanisms by which human tumors arise. Source: Reprinted with permission. Copyright (c) by Scientific American, Inc. [http://www.sciam.com/]. All rights reserved.1 1"Oncogenes," Microsoft(r) Encarta(r) Encyclopedia 2000. (c) 1993-1999 Microsoft Corporation. All rights reserved.
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