Med. Weter. 81
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| JANUSZ A. MADEJ |
| Selected endogenous hormones as inducers of carcinogenesis |
| This review describes cancers arising in hormone-dependent organs and endocrine gland cancers induced by increased hormone secretion, with particular emphasis on the role of estrogens (E) in this process. The carcinogenic effects of E are believed to occur via mitogenic and/or genotoxic pathways. Combining both theories leads to the conclusion that E acts as a „Trojan horse,” transferring carcinogenic metabolites to these hormones (Fig. 2). An additional mechanism of estrogen-induced carcinogenesis is epigenetics, in which genes involved in tumor suppression are silenced and disabled through methylation. The role of „c-onc” oncogenes, mutations, and endogenous carcinogenic reactions leading to carcinogenesis in various organs is also discussed. Mutations in genes responsible for carcinogenesis, caused by increased hormone levels (E, P, FSH, LH), may be responsible for an increased risk of developing cancer in the breast, endometrium, ovary, prostate, or thyroid gland. Similarly, the role of hormones in the transformation of proto-oncogenes into carcinogenic oncogenes is evident in many cancers. Thus, cancers arise as a result of genetic and epigenetic changes within tumor suppressor genes, proto-oncogenes, and „caretaker” genes, such as BRCA1 and hMLH2. Despite morphological changes in cells affected by neoplastic transformation, their ability to recognize hormonal signals is not inhibited, a feature that is exploited in oncotherapy. In addition, the role of surrogate tests of blood and other body fluids as material for molecular diagnosis of cancer, e.g. efDNA, mtDNA, eccDNA, Evs-DNA, miRNA without disturbing the tumor – so-called liquid biopsy – has been described. |
| Keywords: cancer, carcinogenesis, estrogen, proto-oncogene, oncogene |