Cancer and how It Begins
Various inhibitory proteins can restrain forward movement through the cycle. Among them are p15 and p16, both of which clock the activity of the CDK partners of cyclin D, consequently preventing the advance of the cell from G1 into S. Another inhibitor of CDKs, termed p21 is under control of a tumor suppressor protein, p53, which monitors the health of the cell, the reliability of its chromosomal DNA and the successful completion of the different steps in the cycle (Israel, 374).
Breast cancer cells often produce excesses of cyclin D and cyclin E. In many cases of melanoma, skin cells have lost the gene encoding the breaking protein p16. Half of all types of human tumors lack a functional p53 protein. And, in cervical cancers generated by infection of cells with a human papilloma virus, both the pRB and p53 proteins are frequently disabled; eliminating two of the clock's most vital restraints. The end result in all these cases is that he clock begins to spin out of control, ignoring any external warnings to stop. If researchers can develop ways to secure the cyclins and CDKs active in the cell cycle, they may be able to stop the progress of cancer cells in their tracks (Hellman, 286).
So far two ways that tissues normally hold down cell production and avoid cancer have been discussed. They prevent excess multiplication by depriving a cell of growth-stimulatory factors or, on the other hand, by showering it with antiproductive factors. Still, cells on their way to becoming cancerous often avoid these controls: they stimulate themselves and turn a deaf ear to inhibitory signals. …
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