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I.R.F. / Survey / Chapter 3

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Aging, The Molecular Concepts


There is mounting evidence that cellular senescence acts as a "cancer brake" because it takes many divisions to accumulate all the changes needed to become a cancer cell. In addition to the accumulation of several mutations in oncogenes and tumor suppressor genes, almost all cancer cells are immortal and, thus, have overcome the normal cellular signals that prevent continued division. Young normal cells can divide many times; but these cells are not cancer cells since they have not accumulated all the other changes needed to make a cell malignant. In most instances, cells become senescent before they can become a cancer cell. Therefore, aging and cancer are two ends of the same spectrum. The key issue is to find out how to make our cancer cells mortal and our healthy cells immortal, or at least longer lasting. Inhibition of telomerase in cancer cells may be a viable target for anti-cancer therapeutics while expression of telomerase in normal cells may extend lifespan.

The gene for telomerase is both an important target for cancer and for the treatment of age-related disease. The telomerase gene likely will have many important applications in the future of medicine and cellular engineering.

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