Role of programmed cell death in carcinogenesis.
Cells possess within their repertoire of genetic programs the ability not only to proliferate and be functionally active, but also to activate and undergo a process of self-induced destruction. This process, called programmed cell death, involves a genetic reprogramming of the cell that results in an energy-dependent cascade of biochemical and morphological changes within the cell that result in its death and elimination. Activation of this programmed death process is controlled by a series of endogenous cell-type-specific signals. In addition, a variety of exogenous cell-damaging treatments (e.g., radiation, chemicals, and viruses) can activate this pathway if sufficient injury to the cell occurs. Because a cell must undergo a series of molecular changes to acquire the malignant phenotype and because these changes are often induced by agents or treatment that damage the cell over an extended period of time, anything that enhances the survival of initiated/damaged cells will promote the carcinogenic process. This paper presents an overview of the regulation and mechanism of programmed cell death and how derangement of this regulation may be involved in carcinogenesis.
Johns Hopkins Oncology Center, Baltimore, MD 21231.
J T
JT
Isaacs
D000728:Androgens / Q000502:physiology; D000818:Animals; D017209:Apoptosis / Q000187:drug effects / Q000502:physiology*; D002273:Carcinogens / Q000633:toxicity; D002453:Cell Cycle / Q000502:physiology; D002471:Cell Transformation, Neoplastic; D006801:Humans; D008297:Male; D008954:Models, Biological; D009369:Neoplasms / Q000209:etiology* / Q000473:pathology*; D011467:Prostate / Q000166:cytology / Q000502:physiology
D000728:Androgens; D002273:Carcinogens