Ectopic hormone production by malignant tumors.

Malignant tumours of nonendocrine tissues may produce ectopic hormones. The most likely mechanism is depression of genes which code for hormones. Ectopic hormones are invariably peptides, and each is identical to some peptide product of an endocrine gland. However, the majority of ectopic hormones occur as biologically inactive precursors or subunits and therefore remain occult unless they are specifically sought. When appropriate assays are made for such inactive forms, it is found that ectopic production of hormone-like peptides occurs frequently. Clinical syndromes result only in the relatively rare patients in whom a biologically active form is synthesized in large quantities. Laboratory research in this area improves our understanding of genetic control mechanisms in neoplasia. Ectopic hormones may be of limited use in diagnosis of cancer, especially when multiple markers are measured simultaneously.

Induction of aryl hydrocarbon hydroxylase and forestomach tumors ben benzo(a)pyrene.

While papillomatous tumors developed in the forestomach of female Ha/ICR mice after a 12-week chronic feeding period of benzo(a)pyrene (BP), no tumors developed in the glandular portion of stomach or in the lung or liver. Among all tissues examined, the forestomach showed the greatest increase of aryl hydrocarbon hydroxylase (AHH) activity following acute or chronic administration of BP. Single acute doses of BP induced AHH activity in forestomach, glandular stomach, lung, and small intestine, but not in the kidney and liver of these animals. Similarly, after chronic administration of BP, AHH activity was inducible in the forestomach, glandular stomach, and lung, but again not in the liver. Although the formation of tumors is associated with greater inducibility of AHH activity in the forestomach after BP administration, the relationship between tissue inducibility of AHH activity and susceptibility to BP carcinogenesis is still not clear. Further studies regarding the formation of specific carcinogenic epoxides of BP in itssues both susceptible (e.g., forestomach) and resistant to BP carcinogenesis would more clearly define the relationship between AHH inducibility and BP carcinogenesis.