Pathophysiological aspects of tumor development.
Neoplastic transformation is one possible consequence of genomically disturbed intracellular feedback mechanisms normally governing life, differentiation, function and death of an individual cell. Neoplastic growth can be thought of as the abnormal activation of the mitotic program and/or the inactivation of programs for growth-inhibition and apoptosis. This article reviews the current knowledge on three types, or families, of proteins that act on different levels of subcellular organization and are involved in controlling the integrity of the genome, survival and death: i) the DNA-binding nuclear protein p53 inducing cell cycle arrest and apoptosis, ii) the bcl-2 family of proteins acting as regulators of prolonged survival and programmed cell death and iii) APO-1/Fas, a cell surface receptor transducing an apoptotic signal delivered either by the cell itself (cis death) or by another cell (trans death). Although much is still unknown, especially concerning the functional linkages of these three principles, the data available allow a fascinating insight into the society of cells, which we are, after all.
D000818:Animals; D017209:Apoptosis / Q000502:physiology; D006801:Humans; D009369:Neoplasms / Q000209:etiology* / Q000235:genetics / Q000503:physiopathology*; D011518:Proto-Oncogene Proteins / Q000235:genetics / Q000502:physiology; D019253:Proto-Oncogene Proteins c-bcl-2; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000502:physiology; D019014:fas Receptor / Q000502:physiology
D011518:Proto-Oncogene Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D016159:Tumor Suppressor Protein p53; D019014:fas Receptor