Hormonal therapy in cancer of the breast.I. The effect of testosterone propionate therapy on clinical course and hormonal excretion

Segaloff, Albert; Gordon, Douglas; Horwitt, Benjamin N.; Schlosser, Joseph V.; Murison, Paul J.

doi:10.1002/1097-0142(195103)4:2<319::aid-cncr2820040217>3.0.co;2-5

Cited by 51 publications

(11 citation statements)

References 6 publications

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“…Subsequently, the use of testosterone propionate, the testosterone derivative fluoxymesterone and the steroid calusterone obtained promising results in terms of disease response and pain relief in patients with metastatic BC (MBC) whose hormone receptor status was unknown (Segaloff et al 1951, Kennedy 1958, Goldenberg 1964, Goldenberg et al 1973, Gordan et al 1973). More recently, Boni et al reported a significant therapeutic activity of testosterone propionate in a consecutive series of 53 patients with ER/PgR-positive MBC (Boni et al 2014).…”

Section: Ar-targeting Therapy In Bcmentioning

confidence: 99%

Androgen receptor signaling pathways as a target for breast cancer treatment

Pietri¹,

Conteduca²,

Andreis³

et al. 2016

Endocrine-Related Cancer

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The androgen receptor (AR) is a ligand-dependent transcription factor, and its effects on breast range from physiological pubertal development and age-related modifications to cancer onset and proliferation. The prevalence of AR in early breast cancer is around 60%, and AR is more frequently expressed in ER-positive than in ER-negative tumors. We offer an overview of AR signaling pathways in different breast cancer subtypes, providing evidence that its oncogenic role is likely to be different in distinct biological and clinical scenarios. In particular, in ER-positive breast cancer, AR signaling often antagonizes the growth stimulatory effect of ER signaling; in triple-negative breast cancer (TNBC), AR seems to drive tumor progression (at least in luminal AR subtype of TNBC with a gene expression profile mimicking luminal subtypes despite being negative to ER and enriched in AR expression); in HER2-positive breast cancer, in the absence of ER expression, AR signaling has a proliferative role. These data represent the rationale for AR-targeting treatment as a potentially new target therapy in breast cancer subset using androgen agonists in some AR-positive/ER-positive tumors, AR antagonists in triple-negative/ AR-positive tumors and in combination with anti-HER2 agents or with other signaling pathways inhibitors (including PI3K/MYC/ERK) in HER2-positive/AR-positive tumors. Only the ongoing and future prospective clinical trials will allow us to establish which agents are the best option in every specific condition, keeping in mind that there is evidence of opposite androgens and AR agonist/antagonist drug effects on cell proliferation particularly in AR-positive/ER-positive tumors.

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Section: Ar-targeting Therapy In Bcmentioning

confidence: 99%

Androgen receptor signaling pathways as a target for breast cancer treatment

Pietri¹,

Conteduca²,

Andreis³

et al. 2016

Endocrine-Related Cancer

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“…Received for publication September 13, 1956 THE beneficial effects obtained by hypophysectomy in the treatment of advanced cancer of the human breast have revived interest in the role of pituitary factors in the pathogenesis of mammary tumours (Coppedge and Segaloff, 1951;Segaloff, Gordon, Horwitt, Schlosser and Murison, 1951;Scowen and Hadfield, 1955;Hadfield, 1956a and b). Many years ago experimentalists produced evidence for a promoting influence of the adenohypophysis on the growth of mammary cancers in mice.…”

mentioning

confidence: 99%

A New Strain of Mice with a High Incidence of Mammary Cancers and Enlargement of the Pituitary

Bielschowsky¹,

Bielschowsky²,

Lindsay³

1956

Br J Cancer

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THE beneficial effects obtained by hypophysectomy in the treatment of advanced cancer of the human breast have revived interest in the role of pituitary factors in the pathogenesis of mammary tumours (Coppedge and Segaloff, 1951;Segaloff, Gordon, Horwitt, Schlosser and Murison, 1951; Scowen and Hadfield, 1955; Hadfield, 1956a and b). Many years ago experimentalists produced evidence for a promoting influence of the adenohypophysis on the growth of mammary cancers in mice. Morphological descriptions of the pituitary in this condition remain scanty and to our knowledge no pattern has emerged which could be called typical for cancer of the breast. When we came into the possession of a high mammary cancer strain, the pituitaries of which showed gross abnormalities, it was hoped that a useful tool had become available for a reinvestigation of the role of pituitary hormones in the development of tumours of the breast. In the following an account will be given of the origin of this strain (NZY), of the endocrine abnormalities observed in the females and of the neoplasms occurring in animals of both sexes. METHODS AND MATERIALThe mice were kept in thermostatically controlled rooms at a temperature 70 ± 2°F. The composition of the stock diet as well as of the food given to the breeders has been described in a previous communication (Bielschowsky and Bielschowsky, 1956).At the age of 28 days the animals were separated from their mothers and the female offspring from the male. Some of the females were kept as virgins, the others, at the age of 8 weeks, were mated to their brothers with whom they remained until they had produced and reared 4-7 litters. However, when a breeder failed to become pregnant during a period of 3 months the animal was removed from the breeding box.Forty miales, 31 virgins and 84 breeders belonging to the 18th-24th generation were kept under observation during their full life span. They were killed when they appeared to be seriously ill or when palpable tumours were discovered. Some mice with mammary cancers were allowed to live for 5-8 weeks after the tumour was first observed. It was impossible to keep a constant number of animals per box but care was taken to avoid overcrowding. The maximum nunmber of mice at any one time never exceeded 15 in boxes measuring 28 x 43 X 13 cm.The material presented in this paper consists of the 155 mice mentioned above together with 43 healthy females and 6 males killed for a study of the endocrine glands and their target organs.

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“…The alternative was to suppress estrogen pharmacologically, and it was found that this could be achieved by administering testosterone (Mukherjee, 2011). Testosterone soon became an important and effective treatment for breast cancer, and was used extensively between the 1930s and 1960s (Fels, 1944;Goldenberg, 1964;Segaloff et al, 1951Segaloff et al, , 1964. However, when raised blood and urine levels of testosterone were found in breast cancer patients, testosterone was assumed to be the cause and not a simple associated factor, and successful testosterone therapy was abandoned (Malarkey et al, 1977;Secreto et al, 1983).…”

Section: Breast Cancermentioning

confidence: 99%