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Hormonal influences on chemical carcinogenesis: studies with the aflatoxin B1 hepatocarcinoma model in the rat.

Abstract
The role of adrenocorticotropin, cortisol, and corticosterone on chemical carcinogenesis was investigated using the rat aflatoxin B1 hepatocarcinoma model. The animals were divided into untreated controls and various experimental groups receiving the carcinogen alone or the carcinogen with a hormone. Animals lost during the treatment period died mostly of massive hepatic necrosis. The results following 65 weeks of observation show that: (1) hormones decrease the toxicity of aflatoxin B1; (2) adrenocorticotropin possibly exerts its influence on aflatoxin B1 hepatocarcinogenesis through adrenal stimulation, and (3) in aflatoxin B1-adrenocorticotropin treated animals, hepatocellular carcinoma, cholangiocarcinoma, and malignant lymphoma may be observed.
AuthorsA Chedid, C J Halfman, S R Greenberg
JournalDigestive diseases and sciences (Dig Dis Sci) Vol. 25 Issue 11 Pg. 869-74 (Nov 1980) ISSN: 0163-2116 [Print] United States
PMID6254737 (Publication Type: Comparative Study, Journal Article, Research Support, U.S. Gov't, P.H.S.)
Chemical References
  • Aflatoxins
  • Hormones
  • Adrenocorticotropic Hormone
  • Corticosterone
  • Hydrocortisone
Topics
  • Adenoma, Bile Duct (chemically induced)
  • Adrenal Cortex (drug effects)
  • Adrenocorticotropic Hormone (therapeutic use)
  • Aflatoxins (adverse effects, antagonists & inhibitors)
  • Animals
  • Corticosterone (therapeutic use)
  • Disease Models, Animal
  • Hormones (therapeutic use)
  • Hydrocortisone (therapeutic use)
  • Liver Neoplasms (chemically induced)
  • Liver Neoplasms, Experimental (chemically induced, prevention & control)
  • Lymphoma (chemically induced)
  • Male
  • Rats
  • Stimulation, Chemical

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