Angiogenesis and apoptosis are cellular parameters of neoplastic progression in transgenic mouse models of tumorigenesis.
The epidemiology and histopathology of human cancers and studies of animal models of tumorigenesis have led to a widely-accepted notion that multiple genetic and epigenetic changes have to accrue for the successful development of a malignant phenotype. Tumor growth and expansion requires an ability not only to proliferate, but also to down-modulate cell death (apoptosis) and activate angiogenesis to produce a tumor neovasculature. This review will describe the interplay between apoptosis and proliferation, as well as the characteristics of the angiogenic phenotype in two transgenic mouse models of multi-step tumorigenesis, namely, pancreatic islet cell carcinomas and squamous cell carcinomas of the skin.
Bergers
G
G
Department of Biochemistry and Biophysics, and Hormone Research Institute, University of California, San Francisco 94143-0534, USA.
Hanahan
D
D
Coussens
L M
LM
D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D002455:Cell Division; D002471:Cell Transformation, Neoplastic; D004195:Disease Models, Animal; D018450:Disease Progression; D006801:Humans; D051379:Mice; D018345:Mice, Knockout; D008822:Mice, Transgenic; D009369:Neoplasms / Q000473:pathology / Q000503:physiopathology*; D009374:Neoplasms, Experimental / Q000473:pathology / Q000503:physiopathology; D009389:Neovascularization, Pathologic