| Development of cancer chemopreventive drugs based on mechanistic approaches. | |
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MedLine Citation:
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PMID: 16083917 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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One of the most important medical practices of the 21st century is the chemoprevention of cancer. Much progress has been made in this new emerging field, but much work remains before widespread use and practice of cancer prevention becomes commonplace. Cancer chemoprevention includes the concepts of inhibition, reversal, and retardation of the cancer process. The process of carcinogenesis requires 20-40 years to reach invasive cancer. This process follows multiple, diverse, and complex pathways in a stochastic process, called clonal evolution. Many of these pathways appear amenable to inhibition, reversal, or retardation at various points. It is urgent that we identify key pathways in the evolution of the cancer cell, which can be exploited to prevent this carcinogenesis process. Basic researchers are identifying many genetic lesions and epigenetic processes associated with the progression of precancer to invasive disease. These precancer lesions are also called intraepithelial neoplasia (IEN). Many of these early precancerous lesions favor cell division over quiescence and protect cells against apoptosis when signals are present. Many oncogenes, which are active during early development, are reactivated in adulthood by aberrant gene promoting errors. Normal regulatory genes can become mutated, making them insensitive to normal regulatory signals. Tumor suppressor genes are deleted or mutated rendering them inactive. These are several of a wide range of defects in cellular machinery, which can lead to evolution of the cancer phenotype. Errors may not have to appear in a defined order for cells to progress along the cancer pathway. To conquer this diverse disease, it is necessary to attack multiple key pathways at once for a predetermined period of time. Agent combination prevention strategies are, therefore, essential to decrease cancer morbidity. Each cancer type, organ location, or individual genetic background may require a custom combination of prevention strategies to be successful. |
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Authors:
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Vernon E Steele; Gary J Kelloff |
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Publication Detail:
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Type: Journal Article; Review Date: 2005-08-03 |
Journal Detail:
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Title: Mutation research Volume: 591 ISSN: 0027-5107 ISO Abbreviation: Mutat. Res. Publication Date: 2005 Dec |
Date Detail:
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Created Date: 2005-11-23 Completed Date: 2006-09-15 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0400763 Medline TA: Mutat Res Country: Netherlands |
Other Details:
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Languages: eng Pagination: 16-23 Citation Subset: IM |
Affiliation:
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National Cancer Institute, EPN 2108, MSC 7322, 9000 Rockville Pike, National Institutes of Health, Bethesda, MD 20892-7322, USA. vs1y@nih.gov |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Anticarcinogenic Agents
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therapeutic use* Humans Mutation* Neoplasms* / genetics, prevention & control |
| Chemical | |
Reg. No./Substance:
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0/Anticarcinogenic Agents |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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