ras activation in experimental carcinogenesis.
We review experimental models of carcinogenesis in which the role of ras activation has been most thoroughly studied: skin, thymus, mammary gland and liver. Qualitative changes (point mutations), as well as quantitative changes (over-expression, increased gene dosage) contribute to the transforming phenotype induced by ras genes. The activation of the three different ras family members is associated with particular tumor types, carcinogenic agents, and carcinogenic stages, suggesting the ras proteins may be involved in different biological functions. Depending on the system, ras activation has been shown to be an early and/or a late event in the multi-step process of carcinogenesis. These data underscore the possible relationship between ras activation and cell type specificity, proliferation, differentiation or cell-cell interaction.
Mangues
R
R
Department of Pathology and Kaplan Cancer Center, New York University Medical Center, NY 10016.
Pellicer
A
A
D000818:Animals; D002471:Cell Transformation, Neoplastic / Q000235:genetics*; D004195:Disease Models, Animal; D015972:Gene Expression Regulation, Neoplastic; D011905:Genes, ras / Q000502:physiology*; D008114:Liver Neoplasms, Experimental / Q000235:genetics; D008223:Lymphoma / Q000235:genetics; D008325:Mammary Neoplasms, Experimental / Q000235:genetics; D051379:Mice; D009374:Neoplasms, Experimental / Q000235:genetics*; D011817:Rabbits; D012878:Skin Neoplasms / Q000235:genetics