Feminizing interstitial cell tumor of the testis: Personal observations and a review of the literature

Gabrilove, J. Lester; Nicolis, G.L.; Mitty, Harold A.; Sohval, Arthur R.

doi:10.1002/1097-0142(197504)35:4<1184::aid-cncr2820350425>3.0.co;2-z

Cited by 130 publications

(30 citation statements)

References 52 publications

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“…47 Leydig and Sertoli cell tumours are unusual forms of testicular tumours (< 5%) which oestrogenize by secreting oestradiol. 48,49 The oestrogen/androgen ratio in these patients is enhanced by oestradiol inhibition of the activity of 17,20-lyase and 17a -hydroxylase, both of which are critical for the synthesis of testosterone. 50 It is important to note that these tumours may be occult and require the imaging of clinically normal testes.…”

Section: Pathological Gynaecomastia Tumoursmentioning

confidence: 99%

Endocrinology of gynaecomastia

Ismail¹,

Barth²

2001

Ann Clin Biochem

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Gynaecomastia is the most common disorder of the male breast. It can occur at any age, and for this reason laboratory investigations may be requested by clinicians from many specialties. Gynaecomastia may occur transiently in neonates. It may also occur transiently during puberty, when it is common and generally benign. It must, however, be regarded as unusual in prepubertal children and all young and middle-aged men. Although iatrogenic and benign gynaecomastia are common in the elderly, further investigations may still be justi®ed since breast cancer or other neoplasm must be ruled out. Biochemical investigations, when warranted, are aimed at establishing an underlying cause. Endocrine investigations might include serum oestradiol (or oestrone if available), testosterone, luteinizing hormone, sex-hormone-binding globulin, human chorionic gonadotrophin, prolactin and thyroid function tests. In this review, the source and role of oestrogens in men, the androgen±oestrogen dynamics, the causes and clinical entities of gynaecomastia, and interpretation of laboratory tests are described.

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Section: Pathological Gynaecomastia Tumoursmentioning

confidence: 99%

Endocrinology of gynaecomastia

Ismail¹,

Barth²

2001

Ann Clin Biochem

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“…Leydig cell tumour have been associated with gynaecomastia at presentation. Absence of gynaecomastia in an adult patient is said to be another feature suggesting malignancy (Gabrilove et al 1975. Kim et al 1985, Grem et al 1986).…”

Section: Pathological Findingsmentioning

confidence: 99%

“…Our case is unusual in view of associated gynaecomastia. said to indicate benignity, and tumour ossification, previously reported in only one benign Leydig cell tumour (Mikowitz, Soloway & Soscia 1965, Gabrilove et al 1975, Kim et al 1985.…”

Section: Introductionmentioning

confidence: 99%

Ossifying malignant Leydig (interstitial) cell tumour of the testis

Balsitis

Sokal

1990

Histopathology

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“…Thus, in the absence of the opposing effects of androgen, sufficient estrogen is produced by normal men to result in profound breast enlargement. Alternatively, estrogen production can increase above the normal range either because of enhanced testicular secretion of estradiol (as in certain testicular tumors) (5,6) or because of increased formation of estrogen in extraglandular sites (as in cirrhosis of the liver) (2, 7). Since the development of feminizing signs is similar in such fundamentally different disorders, Lewin (8) the ratio of androgen to estrogen, a concept that has received support from detailed studies of androgen and estrogen metabolism in men with feminization in diverse clinical states (2,9).…”

Section: Introductionmentioning

confidence: 99%

Antiestrogenic action of dihydrotestosterone in mouse breast. Competition with estradiol for binding to the estrogen receptor.

Casey¹,

Wilson²

1984

J. Clin. Invest.

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A bstract. Feminization in men occurs when the effective ratio of androgen to estrogen is lowered. Since sufficient estrogen is produced in normal men to induce breast enlargement in the absence of adequate amounts of circulating androgens, it has been generally assumed that androgens exert an antiestrogenic action to prevent feminization in normal men. We examined the mechanisms of this effect of androgens in the mouse breast.Administration of estradiol via silastic implants to castrated virgin CBA/J female mice results in a doubling in dry weight and DNA content of the breast. The effect of estradiol can be inhibited by implantation of 17#-hydroxy-5a-androstan-3-one (dihydrotestosterone), whereas dihydrotestosterone alone had no effect on breast growth. Estradiol administration also enhances the level of progesterone receptor in mouse breast. Within 4 d of castration, the progesterone receptor virtually disappears and estradiol treatment causes a twofold increase above the level in intact animals. Dihydrotes inhibits estradiol-mediated induction of the progesterone receptor. Dihydrotestosterone also promotes the translocation of estrogen receptor from cytoplasm to nucleus; the ratio of cytoplasmic-to-nuclear receptor changes from 3:1 in the castrate to 1:2 in dihydrotestosteronetreated mice. Thus, the antiestrogenic effect of androgen in mouse breast may be the result of effects of dihydrotestosterone on the estrogen receptor. If so, dihydrotestosterone performs one of its major actions independent of the androgen receptor. IntroductionNormal men produce -45 ,ug of estradiol each day, a sixth of which is secreted by the testes and the remainder of which is derived from the extraglandular aromatization of circulating androgens (1). Extraglandular estradiol formation takes place by two mechanisms, one from the direct conversion of testosterone to estradiol and the other from androgens of adrenal origin by the sequence of androstenedione -estrone -estradiol. The function of estradiol in normal men is unknown, but feminization, commonly manifested by gynecomastia, ensues under conditions of relative or absolute estrogen excess (2).Relative estrogen excess occurs when the synthesis or action of androgen is impaired but estrogen production is maintained at or near normal (as occurs in testicular regression or in testicular failure when testicular androgen production ceases but the formation of estrogens from adrenal androgens is unimpaired (3,4] The mechanism by which androgen inhibits estrogen action is unknown. Evidence has been developed in the MCF7 cell line that 17,3-hydroxy-5a-androstan-3-one (dihydrotestosterone)' functions as an antiestrogen by binding to the estrogen receptor itself and like certain other antiestrogens, that dihydrotestosterone can act as a weak estrogen in high concentration (10). Alternatively, the antiestrogenic actions of androgen on the embryonic mouse breast (11) and on the rodent uterus (12) appear to be mediated via the androgen receptor, e.g., androgen induces some action at the ge...

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Feminizing interstitial cell tumor of the testis: Personal observations and a review of the literature

Cited by 130 publications

References 52 publications

Endocrinology of gynaecomastia

Endocrinology of gynaecomastia

Ossifying malignant Leydig (interstitial) cell tumour of the testis

Antiestrogenic action of dihydrotestosterone in mouse breast. Competition with estradiol for binding to the estrogen receptor.

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