Steroid—receptor interaction in a canine anal adenoma

Abstract

An anal adenoma from a dog has been examined for cytosol binding proteins for androgens and oestrogens. Sucrose‐density gradient analysis revealed low capacity binding moieties for testosterone with sedimentation coefficients of 2S and 8S, for 5α‐dihydrotestosterone (8S) and for oestradiol‐17β (4S and 8S). In each case it was shown that the steroids could be translocated to the nuclei and were found there to be protein‐bound. The dissociation constants for 5α‐dihydrotestosterone and oestradiol‐17β were 5×1 × 10‐10M and 2×6 × 10‐10M respectively and the corresponding receptor site concentrations were 9 and 38 fmol/mg cytosol protein. The possible significance of these findings with regard to the induction and maintenance of such tumours is discussed.

Sex Steroid Hormones and Tumors in Domestic Animals

“…To better understand this relationship, recent research has focussed on pinpointing the site of action of these hormones and on locating their receptors in both normal and tumour tissues. As a result, biochemical and immunohistochemical studies carried out over the last few years have detected androgen receptors (AR), oestrogen receptor α (ERα) and progesterone receptors (PR) in epidermis, hair follicles and fundamentally in the sebaceous glands of canine skin [113][114][115][116][117]. These results suggest that not only androgens and oestrogens, but also progesterone, may play a major role in the regulation of normal skin appendage function and in the pathogenesis and development of neoplasms.…”

“…This evidence has for years been interpreted as proof of a clear stimulation of tumour development by sex steroid hormones, particularly androgens [123]. Adenomas have been found to be hormoneresponsive; a full or partial regression has been observed following castration or oestrogen treatment [113,120,124]. In females, perianal adenomas occur almost exclusively in ovariohysterectomised animals whose low oestrogen levels fail to suppress tumour growth.…”

Immunohistochemical Detection of Growth Hormone (GH) in Canine Hepatoid Gland Tumors

“…In contrast, hepatoid gland carcinomas (perianal gland carcinomas) are much less frequent than benign counterpart [19]. On the basis of the presence of androgen and estrogen hormone receptors [3,17] and of a good post-surgical response to orchiectomy [18], it is generally accepted that hepatoid gland tumors represent an hormone-dependent system. Growth hormone (GH) expression has been reported in extrapituitary sites during normal and pathological conditions in other hormone-dependent settings such as hyperplastic and neoplastic mammary tissues of bitches [13,16], in normal canine prostate [5] and in cystic endometrial hyperplasia [8].…”

“…It was reported that hepatoid glands possessed sex hormone receptors [3,17] suspecting to be hormone dependent was suspected. In support of the observation, castration has long been a common practice to control hepatoid gland tumors [18].…”

>b<Avaliação da concordância interobservadores de critérios morfológicos no diagnóstico de tumores de glândula hepatoide em cães e determinação do valor prognóstico de aspectos clínico-patológicos e marcadores imuno-histoquímicos>/b<

“…Por outro lado, a maior prevalência destes tumores em fêmeas castradas sugere um fator protetor dos estrógenos HAYES, 1979;ASSUNÇÃO, 2003). Alguns estudos têm demonstrado a presença de receptores para andrógenos (testosterona e 5α-dihidrotestosterona) e estrógenos (estradiol-17β) em células hepatoides, os quais apresentam uma maior imunoexpressão em tecidos hiperplásicos quando comparados com os tecidos normal ou neoplásico (CHAISIRI; PIERREPOINT, 1979;PISANI et al, 2006). A eficiência quimioterápica do hormônio sintético dietilestilbestrol também acompanha esta tese, possivelmente exercendo seu efeito não apenas pela ação direta em receptores estrogênicos das células tumorais, mas também pela inibição da secreção de LH pela hipófise e, consequentemente, diminuição da produção de testosterona testicular (RIVIERE;PAPICH, 2018).…”