Endocrinological Study of the Dopaminergic Regulation of Prolactin Release in Metastatic Breast Cancer

Aims and Background Prolactin (PRL) may be a growth factor for breast cancer. Abnormally high levels of PRL have been proven to be associated with a poor prognosis in metastatic breast cancer. However, most studies have been limited to the evaluation of basal levels of PRL rather than its response to the classical endocrine dynamic tests. This study was performed to analyse the dynamic secretion of PRL under stimulatory and inhibitory tests in metastatic breast cancer. Methods The study included 10 untreated metastatic breast cancer women, who were evaluated after the classical stimulatory and inhibitory tests for PRL secretion with the antidopaminergic agent Metoclopramide (10 mg iv as a bolus) and with L-dopa, respectively. Serum levels of PRL were measured by RIA before and at subsequent intervals after drug administration. PRL levels were considered to be elevated when they were higher than 25 ng/ml. Results Abnormally high basal levels of PRL were seen in 6/10 patients. L-dopa was unable to inhibit PRL secretion, whose mean concentrations paradoxically significantly increased in response to L-dopa, with values comparable to those observed after the classical stimulatory test with metoclopramide. Conclusions This study confirm the existence of hyperprolactinemia associated with metastatic breast cancer. In addition, by showing a paradoxical rise of PRL in response to L-dopa, which inhibits PRL secretion in physiological conditions, this study would suggest that breast cancer-related hyperprolactinemia may depend at least in part on endogenous disease-related neuroendocrine alterations.

[1]  Charles B. Wilson,et al.  The Case for Initial Surgical Removal of Certain Prolactinomas , 1997 .

[2]  D. Johnson,et al.  The growth inhibitory properties of a dopamine agonist (SKF 38393) on MCF-7 cells. , 1995, Anti-cancer drugs.

[3]  J. Tomaszewski,et al.  Expression of prolactin and prolactin receptor in human breast carcinoma. Evidence for an autocrine/paracrine loop. , 1995, The American journal of pathology.

[4]  B. Jankovič,et al.  Neuroimmunomodulation From Phenomenology to Molecular Evidence a , b , 1994 .

[5]  D. Giri,et al.  Plasma prolactin as an indicator of disease progression in advanced breast cancer , 1990, Cancer.

[6]  J. Bonneterre,et al.  Prolactin receptors (PRL-R) and breast cancer. , 1989, European journal of cancer & clinical oncology.

[7]  V. Vinnitsky Neurohumoral Mechanisms of the Formation of Antitumoral Activity , 1988, Annals of the New York Academy of Sciences.

[8]  S. Barni,et al.  Prolactin Response to Thyrotropin-Releasing Hormone in Early and Advanced Human Breast Cancer , 1986, Tumori.

[9]  H. Rauschecker,et al.  Hyperprolactinemia is an indicator of progressive disease and poor prognosis in advanced breast cancer , 1984, International journal of cancer.

[10]  H. Nagasawa,et al.  Prolactin and murine mammary tumorigenesis: a review. , 1977, Cancer research.

[11]  Ward Hw Combined anti-prolactin and anti-oestrogen therapy for breast carcinoma. , 1977 .

[12]  H. Ward Combined anti-prolactin and anti-oestrogen therapy for breast carcinoma. , 1977, Clinics in oncology.

[13]  A. Barrett,et al.  Bromocriptine in the treatment of advanced breast cancer. , 1976, Clinical oncology.