New therapies for relapsed castration-resistant prostate cancer based on peptide analogs of hypothalamic hormones

Abstract

It is a pleasure to contribute our presentation at the International Prostate Forum of the Annual Meeting of the American Urological Association (AUA) to this special issue of the Asian Journal of Andrology.

NOTE: Quote from this publication: " [...] We showed that MIA‐602 and our other GHRH antagonists inhibited growth of PC‐3 and 22Rv1 human androgen‐independent prostate cancer cell lines and also hormone‐dependent prostate cancer lines. Our GHRH antagonists also suppressed prostate, kidney, urothelial, breast, triple‐negative breast, ovary, astrocytoma, melanoma, ENT tumors, esophagus, stomach, colon, lung, adrenal cortical, pheochromocytoma, uterus, osteosarcomas and multiple lymphoma types. In addition to their inherent effects on cancer, we found that the GHRH antagonists also potentiated the effects of cytotoxic chemotherapy without enhancing the toxicity! [...]".

Well, now we read as reported a long (!) time ago by "another author":

Quote: "...abnormal cellular growth is depressed in the blast or immature myeloid or lymphoid cells [...]. The growth of lung, stomach and breast cancer, as well as of lymphoma and bone sarcoma is equally depressed or discontinued, so that the survival time of patients is longer and the symptoms become increasingly less severe. In cancer patients the regulatory influence on cellular growth by MLT is strongly strengthened by simultaneous lowering of the level of circulating GH (by means of somatostatin [...]) and prolactin.". Prof. Luigi Di Bella: "Perspectives in pineal functions". Progress in Brain Research, vol. 52, Editors J. Ariens Kappers and P. Pever: 1979.

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See also Somatostatin in oncology, the overlooked evidences in the "Some additional publications about hGH/GH-GHRH/GHRF/GRF" section.