Hormonal carcinogenesis: a novel hypothesis for the role of hormones.
A testable hypothesis on the role of hormones in carcinogenic processes is presented. The hypothesis has been based on the findings that (1) hormones regulate cell division in normal cells, (2) successful neoplastic transformation requires hormonal stimulation of cells receiving carcinogenic insult, (3) normal cells have finite divisional capabilities, whereas neoplastic cells possess infinite divisional capabilities, and (4) normal cells, when present in high ratio, inhibit the growth of neoplastic cells. According to the hypothesis, hormones are considered to be neither mutagenic nor carcinogenic. (Carcinogen is defined as an agent which initiates normal-to-neoplastic transformation). Instead, they play a dual role in carcinogenesis. First, hormones are considered necessary for the fixation of the cell genome neoplastically transformed by carcinogens. Second, hormones, by enhancing the rate of cell division, shorten the life span of normal cells, thus causing a reduction of the normal- to tumor-cell ratio in the population--a condition which facilitates growth of tumor cells.
D000818:Animals; D002471:Cell Transformation, Neoplastic; D005260:Female; D006728:Hormones / Q000494:pharmacology / Q000502:physiology*; D008321:Mammary Glands, Animal / Q000166:cytology / Q000254:growth & development; D009153:Mutagens; D009369:Neoplasms / Q000209:etiology*; D009374:Neoplasms, Experimental / Q000503:physiopathology
D006728:Hormones; D009153:Mutagens