Prolactin Dependence in Human Breast Cancers

Salih, H.; Flax, H.; Brander, W. L.; Hobbs, J.R.

doi:10.1016/s0140-6736(72)92713-4

Cited by 67 publications

(23 citation statements)

References 6 publications

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“…Among the responses are increased synthesis of DNA (Salih et al 1972, Welsch et al 1976, Peyrat et al 1984, Calaf et al 1986), protein (Burke & Gaffney 1978 and α-lactalbumin (Wilson et al 1980), colony formation (Malarkey et al 1983, Manni et al 1986) and changes in shape, adhesion, lipid accumulation (Shiu & Paterson 1984) and estrogen receptor (ER) content (Shafie & Grantham 1981). Increased growth is observed when primary breast biopsy samples are grown in nude mice supplemented with PRL (McManus & Welsch 1984).…”

Section: Prolactin Effects In Vitromentioning

confidence: 99%

Prolactin involvement in breast cancer.

Vonderhaar

1999

Endocrine-Related Cancer

122

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Normal development and differentiation of the mammary gland are profoundly influenced by prolactin (PRL). In rodent mammary cancer PRL plays a well defined role, but its role in human breast cancer has not been appreciated until recently. It is now clear that breast tissue, both normal and malignant, is a significant source of extrapituitary PRL. Thus an autocrine/paracrine role of PRL in human breast cancer may be invoked. Both PRL and PRL receptor mRNA are expressed in the vast majority of breast cancer biopsies independent of estrogen and progesterone receptor status. An autocrine/ paracrine PRL acting in human breast cancer requires that this hormone's action be blocked at the cellular level, as opposed to suppressing the synthesis and secretion of pituitary PRL. Mutants of PRL or human growth hormone are being explored which act as selective PRL antagonists. In addition, tamoxifen has been shown to act locally at the target tissue by binding directly to the PRL receptor and thus inhibiting PRL's action. These strategies may have clinical relevance in treating PRL- Endocrine-Related Cancer (1999) 6 389-404 responsive human breast cancer.

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Section: Prolactin Effects In Vitromentioning

confidence: 99%

Prolactin involvement in breast cancer.

Vonderhaar

1999

Endocrine-Related Cancer

122

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“…These approaches have been reviewed in an earlier report [4] and include studies of steroids on isocitrate dehydrogenase activity [10], tissue respira tion [16], amino acid incorporation [9], 32P uptake [20], acid phosphatase and lactic acid dehydrogenase activity [19], glucose-6-phosphate dehydro genase [8,17,18], and morphology of tumors in short-term culture [5,14,15,19].…”

Section: Others Have Examined the Effect Of Steroids On The Tumor Celmentioning

confidence: 99%

<i>In vitro </i>Assay for Human Breast Cancer Hormone Responsiveness

Burstein¹,

Carey²

1974

Oncology

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Primary or metastatic breast carcinoma from 25 patients was studied in vitro for the effect of Cortisol, estradiol, progesterone, and testosterone on uptake of ^3H-labeled thymidine into tumor cells. In 23 of these cases an objective clinical response of the tumors to endocrine therapy correlated with the in vitro result. All eight patients whose tumors did not respond in vitro did not respond clinically to endocrine manipulation. Of the 15 patients whose tumors were affected in vitro, 9 had a significant clinical response lasting at least 6 months. The assay appears to select hormonal sensitive tumors from those not affected by any hormonal agent. The specific hormonal responsiveness in vitro correlated with the clinical response to ablative endocrine surgery, tumor exacerbation, or response to exogenous steroid hormones in many but not all tumors.

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“…Indeed, the administration of oestrogens to male patients has been reported to result in an increase in breast cancer development (O'Grady and McDivitt, 1969). Although prolactin has been implicated in cancerigenesis of the human female breast (Salih et al, 1972;Kwa et al, 1974), it remains to be determined whether or not this hormone has a role in tumorigenesis of the human male breast. The results of this study provide convincing evidence that in the male rat treated with carcinogenic hydrocarbons, an elevation in the secretion of prolactin significantly increases mammary carcinogenesis.…”

Section: Resultsmentioning

confidence: 99%

Enhancement by prolactin of carcinogen induced mammary cancerigenesis in the male rat

Welsch¹,

Louks²,

Fox

et al. 1975

Br J Cancer

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Summary.-Mammary tumours were induced in 3 groups of male Long-Evans rats by a series of 6 fortnightly gastric intubations of 7, 12-dimethylbenzanthracene. Two weeks before the initial carcinogen treatment one group of rats was grafted with 3 pituitary homografts underneath the kidney capsule of each recipient (hyperprolactinaemia). A second group, 2 weeks before the initial carcinogen treatment and for the duration of the study (35 weeks), were injected 4x weekly with 2-Br-oaergocryptine (CB-154) (hypoprolactinaemia). A third group of rats served as controls. A significant increase in the incidence of mammary tumours and a reduced latency period of tumour appearance in the hyperprolactinaemia group, when compared with the controls, were observed in this study. Mammary tumour incidence and latency period of tumour appearance in the hypoprolactinaemia group, however, did not differ significantly from controls. Thus, an increased secretion of pituitary prolactin in rats appears to be an important enhancing endocrinic condition in carcinogenesis of the male mammary gland.

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Prolactin Dependence in Human Breast Cancers

Cited by 67 publications

References 6 publications

Prolactin involvement in breast cancer.

Prolactin involvement in breast cancer.

<i>In vitro </i>Assay for Human Breast Cancer Hormone Responsiveness

Enhancement by prolactin of carcinogen induced mammary cancerigenesis in the male rat

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