title: [Testosterone production by tumor tissue in partial androgen deficiency in aged men (PADAM)].
abstract: The aim of the study was examination of cause-effect relationships between PADAM, extragonadal production of androgens and high proliferative activity in aged men. The study group included 15 patients aged between 53 and 79 years with prostatic cancer (n = 5), urinary bladder cancer (n = 5) and cancer of the rectum (n = 5). Control samples of tissues of the prostatic gland, urinary bladder and rectum were obtained from dead bodies of men at the age between 18 and 29 years killed in the accidents at the age from 18 to 29 years. Testosterone levels in the tissues of peritumor zone of the prostate, in tumor tissue of patients with cancer of the prostate, urinary bladder and the rectum were higher than in blood serum. In prostatic cancer, testosterone in the tumor tissue was higher than in the tissues of prostatic peritumor zone. The values of Histochemical score AR of the peritumor zone in prostatic cancer patients were higher than those of the control group. It was detected that ER, PR, bcl-2, Ki-67 and p53 in prostatic tissue of young controls were absent while in patients with prostatic cancer these factors were expressed in the peritumor zone. In cancer of the urinary bladder, peritumor zone showed expression of PR, bcl-2, Ki-67 and p53, while no such expression was in the controls. ER, bcl-2, Ki-67 and p53 were registered in the peritumor zone of patients with cancer of the rectum but the controls had neither ER, bcl-2 nor p53 while Ki-67 expression in rectal cancer was higher than in the controls. The results of the study suggest that testosterone production by some tumors and tissues of the peritumor zone accompanied with high proliferative activity and dysregulation of the cell cycle is secondary to PADAM. These changes arise to compensate testicular deficiency and are manifestations of metabolic syndrome (X-syndrome). In this situation immune system fails to utilize all atypical cells.
authors.forename: A V
authors.initials: AV
authors.lastname: Pecherskiĭ
authors.forename: V F
authors.initials: VF
authors.lastname: Semiglazov
authors.forename: B K
authors.initials: BK
authors.lastname: Komiakov
authors.forename: B G
authors.initials: BG
authors.lastname: Guliev
authors.forename: A I
authors.initials: AI
authors.lastname: Gorelov
authors.forename: A I
authors.initials: AI
authors.lastname: Novikov
authors.forename: V I
authors.initials: VI
authors.lastname: Pecherskiĭ
authors.forename: N N
authors.initials: NN
authors.lastname: Simonov
authors.forename: A V
authors.initials: AV
authors.lastname: Guliaev
authors.forename: I A
authors.initials: IA
authors.lastname: Samusenko
mesh_terms: D000293:Adolescent; D000328:Adult; D000367:Age Factors; D000368:Aged; D000728:Androgens / Q000172:deficiency*; D006729:Hormones, Ectopic / Q000096:biosynthesis*; D006801:Humans; D019394:Ki-67 Antigen / Q000032:analysis; D008297:Male; D008875:Middle Aged; D009369:Neoplasms / Q000737:chemistry / Q000378:metabolism*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000032:analysis; D011960:Receptors, Estrogen / Q000032:analysis; D011980:Receptors, Progesterone / Q000032:analysis; D013739:Testosterone / Q000032:analysis / Q000096:biosynthesis*; D016159:Tumor Suppressor Protein p53 / Q000032:analysis
chemical_list: D000728:Androgens; D006729:Hormones, Ectopic; D019394:Ki-67 Antigen; D019253:Proto-Oncogene Proteins c-bcl-2; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone; D016159:Tumor Suppressor Protein p53; D013739:Testosterone