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Tumor Suppressor Genes

  • Dennis W. Ross
Chapter
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Abstract

This is an oversimplification of the myriad of molecular functions under the control of these genes. Proto-oncogenes,as we discussed in the last chapter, encode for proteins in the cell signaling pathway and apoptosis. When mutated into oncogenes, their function results in an unregulated stimulation of cell division. Mutated oncogenes act in a dominant genetic mode, producing an abnormal phenotype, even though a second allele of the gene is not mutated. Tumor suppressor genes (at one time called antioncogenes) have the normal physiologic role of retarding cell division. Tumor suppressor genes differ from oncogenes in several other ways besides their opposing effects on cell division. Tumor suppressor genes do not exist in a viral form, as is the case for oncogenes. This should not be surprising. A retrovirus benefits from carrying an oncogene along in its genome to promote division in cells it infects. There would be no benefit to a virus in carrying a copy of a tumor suppressor gene to retard cell division. Tumor suppressor genes work with the DNA repair system, so necessary in maintaining the stability of the genome. Tumor suppressor genes in mutated form can be passed on as germline heritable DNA defects. They are the cause of the syndromes of genetic predisposition to cancer. However, tumor suppressor gene mutations occur more commonly as sporadic somatic cell mutations in nonfamilial cancers. Tumor suppressor genes are recessive. Both copies of the gene must be mutated to produce the phenotype: failure to inhibit growth of damaged cells. Table 4.1 lists these contrasting features of oncogenes and tumor suppressor genes.

Keywords

Tumor Suppressor Gene Genetic Mode Human Papilloma Virus Random Mutation Cell Division Cycle 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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References

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Copyright information

© Springer Science+Business Media New York 1998

Authors and Affiliations

  • Dennis W. Ross
    • 1
  1. 1.Department of PathologyForsyth Medical CenterWinston-SalemUSA

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