| Evolutionary maintenance of oncogenesis. | |
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MedLine Citation:
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PMID: 18512072 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: Transformation of normal cells into cells with malignant phenotypes is often the result of loss of tumor suppressor gene (TSG) function after exposure to a carcinogen. CONCLUSIONS: We propose that TSGs susceptible to mutation and consequent loss of function are evolutionarily preserved in normal cell genomes so that the cells survive mutation-inducing insults and thereby evade apoptosis. While the mutations produced in TSGs confer cellular persistence and preclude apoptosis, oncogenesis is the untoward consequence. Proto-oncogenes might similarly be maintained and contain evolutionarily selected and fixed sequences susceptible to mutations (oncogene activation) that prevent cell death but ironically result in host death from malignancy. |
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Authors:
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Steven M Sorscher; Aubrey Hill; Eric J Sorscher |
Publication Detail:
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Type: Journal Article; Review Date: 2008-05-30 |
Journal Detail:
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Title: Journal of cancer research and clinical oncology Volume: 135 ISSN: 0171-5216 ISO Abbreviation: J. Cancer Res. Clin. Oncol. Publication Date: 2009 Jan |
Date Detail:
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Created Date: 2008-11-21 Completed Date: 2009-03-10 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 7902060 Medline TA: J Cancer Res Clin Oncol Country: Germany |
Other Details:
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Languages: eng Pagination: 159-62 Citation Subset: IM |
Affiliation:
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Internal Medicine/Oncology Section, Washington University, Campus Box 8056, St. Louis, MO, 63110, USA. ssorsche@im.wustl.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Cell Transformation, Neoplastic Evolution* Humans Neoplasms / etiology* Oncogenes / physiology* |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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