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Original Studies |
INSERM Unité 344, Faculté Medecine Necker (Ph.T., J-F.M., F.L., M-C.P.V., P.A.K.), 75730 Paris Cedex 15, France; Institut Curie (B.Z., A.N.), 75005 Paris, France; Clinique St. Jean de Dieu (J-C.D.), 75007 Paris, France; Département dEndocrinologie, Hôpital Necker (C.M., F.K.), Paris, France; Laboratoire dExplorations Hormonales, Hôpital Necker (C.T.), 75015 Paris, France
Address all correspondence and requests for reprints to: Philippe Touraine, INSERM Unité 344, Faculté Medecine Necker, 156 rue de Vaugirard, 75730 Paris Cedex 15, France.
The role of PRL in human breast tumorigenesis is not well understood. One of the limitations is the difficulty of accurately measuring PRL receptors (PRLR) in human tissues. We established a quantitative PCR method (Q-PCR) in T-47D human breast cancer cells and applied it to 29 patients, 25 of whom presented with either cancer or fibroadenoma. Four patients underwent a mammoplasty, and normal epithelial cells were cultured before Q-PCR. In T-47D cells, 31 x 106 messenger RNA molecules were detected per microgram of total RNA. In all patients, expression of the PRLR gene was detected, varying from 1500 to 1 x 106 molecules/µg of RNA in normal tissues and from 4500 to 34.7 x 106 molecules/µg of RNA in tumors. PRLR expression was always greater in tumor than in normal contiguous tissue and similar in cultured mammary epithelial cells and normal breast tissues. Estradiol and progesterone receptor-negative tumors expressed low levels of PRLR transcripts, similar to normal breast tissue from menopausal women. Immunocytochemical analysis of PRLR confirmed stronger staining in almost all tumor samples compared with normal tissues. A messenger RNA encoding locally produced human PRL was also identified by RT-PCR in every sample tested. Our results confirm PRLR gene expression in all tissues studied, and moreover, indicate that this expression is increased in human breast tumors vs. normal contiguous tissues.
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