Genomic Instability and Its Role in Neoplasia View Full Text


Ontology type: schema:Chapter     


Chapter Info

DATE

1997

AUTHORS

T D Tlsty

ABSTRACT

The study of how genomic integrity is regulated is important not only in the formation and progression of a neoplasia, but also in how a tumor responds to therapy. Genomic instability has been hypothesized to be a driving force behind multistep carcinogenesis (Nowell 1976). A number of genetic changes are required for a normal cell to become tumorigenic (Foulds 1959; Fearon and Vogelstein 1990). If genomic instability increases the rate at which these alterations occur, then the accumulation of changes and subsequent selection for growth and motility advantage may lead to the formation of a neoplasia. Thus, the new variants generated during tumor progression may be fueled by an underlying genomic instability. Once a cell becomes neoplastic, its evolution may continue to malignancy. Further genetic changes are required to confer metastatic properties on the tumor cell. These properties include the ability to invade surrounding tissues, enter the vasculature, extravasate, and colonize a secondary site. Proficiency at each step is necessary for a tumor cell to become fully metastatic. Genetic alterations are the basis for this acquired variation (Rubin 1987; Liotta et al. 1987). The emergence of drug-resistant or radiation-resistant variants is one of the most disappointing aspects of treating a neoplasia. These variants are generated by the same forces that allow the tumor to become established and progress. More... »

PAGES

37-46

Book

TITLE

Genetic Instability and Tumorigenesis

ISBN

978-3-642-64434-4
978-3-642-60505-5

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/978-3-642-60505-5_4

DOI

http://dx.doi.org/10.1007/978-3-642-60505-5_4

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PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/8979439


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65 schema:description The study of how genomic integrity is regulated is important not only in the formation and progression of a neoplasia, but also in how a tumor responds to therapy. Genomic instability has been hypothesized to be a driving force behind multistep carcinogenesis (Nowell 1976). A number of genetic changes are required for a normal cell to become tumorigenic (Foulds 1959; Fearon and Vogelstein 1990). If genomic instability increases the rate at which these alterations occur, then the accumulation of changes and subsequent selection for growth and motility advantage may lead to the formation of a neoplasia. Thus, the new variants generated during tumor progression may be fueled by an underlying genomic instability. Once a cell becomes neoplastic, its evolution may continue to malignancy. Further genetic changes are required to confer metastatic properties on the tumor cell. These properties include the ability to invade surrounding tissues, enter the vasculature, extravasate, and colonize a secondary site. Proficiency at each step is necessary for a tumor cell to become fully metastatic. Genetic alterations are the basis for this acquired variation (Rubin 1987; Liotta et al. 1987). The emergence of drug-resistant or radiation-resistant variants is one of the most disappointing aspects of treating a neoplasia. These variants are generated by the same forces that allow the tumor to become established and progress.
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