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Abstract:

The etiology of pituitary adenomas remains largely unknown, with the exception of involvement of estrogens in the formation of prolactinomas. We have examined the molecular pathogenesis of prolactin-producing pituitary adenomas in transgenic female mice expressing the human choriongonadotropin (hCG) β-subunit. The LH/CG bioactivity is elevated in the mice, with consequent highly stimulated ovarian progesterone (P4) production, in the face of normal estrogen secretion. Curiously, despite normal estrogen levels, large prolactinomas developed in these mice, and we provide here several lines of evidence that the elevated P4 levels are involved in the growth of these estrogen-dependent tumors. The antiprogestin mifepristone inhibited tumor growth, and combined postgonadectomy estradiol/P4 treatment was more effective than estrogen alone in inducing tumor growth. Evidence for direct growth-promoting effect of P4 was obtained from cultures of primary mouse pituitary cells and rat somatomammotroph GH3 cells. The mouse tumors and cultured cells revealed stimulation of the cyclin D1/cyclin-dependent kinase 4/retinoblastoma protein/transcription factor E2F1 pathway in the growth response to P4. If extrapolated to humans, and given the importance of endogenous P4 and synthetic progestins in female reproductive functions and their pharmacotherapy, it is relevant to revisit the potential role of these hormones in the origin and growth of prolactinomas. © 2010 Society for Endocrinology.

Registro:

Documento: Artículo
Título:Enhanced LH action in transgenic female mice expressing hCGβ-subunit induces pituitary prolactinomas; the role of high progesterone levels
Autor:Ahtiainen, P.; Sharp, V.; Rulli, S.B.; Rivero-Müller, A.; Mamaeva, V.; Röyttä, M.; Huhtaniemi, I.
Filiación:Department of Physiology, University of Turku, FIN-20520 Turku, Finland
Turku Graduate School of Biomedical Science, University of Turku, FIN-20520 Turku, Finland
Department of Surgery and Cancer, Imperial College London, Hammersmith Campus, Du Cane Road, London W12 0NN, United Kingdom
Institute of Biology and Experimental Medicine-CONICET, Vuelta de Obligado 2490, Buenos Aires 1428, Argentina
Department of Pathology, University of Turku, FIN-20520 Turku, Finland
Palabras clave:bromocriptine; chorionic gonadotropin beta subunit; cyclin D1; cyclin dependent kinase 4; estradiol; luteinizing hormone; mifepristone; progesterone; retinoblastoma protein; tamoxifen; transcription factor E2F1; chorionic gonadotropin beta subunit; cyclin dependent kinase 4; luteinizing hormone; progesterone; prolactin; animal cell; animal experiment; animal model; article; cell culture; controlled study; female; gonadectomy; histology; hypophysis tumor; immunohistochemistry; mouse; nonhuman; ovary; progesterone release; prolactinoma; radioimmunoassay; rat; reverse transcription polymerase chain reaction; transgenic mouse; tumor growth; analysis of variance; animal; blood; cell proliferation; cytology; genetics; hypophysis; hypophysis tumor; metabolism; prolactinoma; Analysis of Variance; Animals; Cell Proliferation; Cells, Cultured; Chorionic Gonadotropin, beta Subunit, Human; Cyclin-Dependent Kinase 4; Female; Luteinizing Hormone; Mice; Mice, Transgenic; Pituitary Gland; Pituitary Neoplasms; Progesterone; Prolactin; Prolactinoma; Radioimmunoassay; Reverse Transcriptase Polymerase Chain Reaction
Año:2010
Volumen:17
Número:3
Página de inicio:611
Página de fin:621
DOI: http://dx.doi.org/10.1677/ERC-10-0016
Título revista:Endocrine-Related Cancer
Título revista abreviado:Endocr.-Relat. Cancer
ISSN:13510088
CODEN:ERCAE
CAS:bromocriptine, 25614-03-3; cyclin dependent kinase 4, 147014-97-9; estradiol, 50-28-2; luteinizing hormone, 39341-83-8, 9002-67-9; mifepristone, 84371-65-3; progesterone, 57-83-0; tamoxifen, 10540-29-1; prolactin, 12585-34-1, 50647-00-2, 9002-62-4; Chorionic Gonadotropin, beta Subunit, Human; Cyclin-Dependent Kinase 4, 2.7.11.22; Luteinizing Hormone, 9002-67-9; Progesterone, 57-83-0; Prolactin, 9002-62-4
Registro:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_13510088_v17_n3_p611_Ahtiainen

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Citas:

---------- APA ----------
Ahtiainen, P., Sharp, V., Rulli, S.B., Rivero-Müller, A., Mamaeva, V., Röyttä, M. & Huhtaniemi, I. (2010) . Enhanced LH action in transgenic female mice expressing hCGβ-subunit induces pituitary prolactinomas; the role of high progesterone levels. Endocrine-Related Cancer, 17(3), 611-621.
http://dx.doi.org/10.1677/ERC-10-0016
---------- CHICAGO ----------
Ahtiainen, P., Sharp, V., Rulli, S.B., Rivero-Müller, A., Mamaeva, V., Röyttä, M., et al. "Enhanced LH action in transgenic female mice expressing hCGβ-subunit induces pituitary prolactinomas; the role of high progesterone levels" . Endocrine-Related Cancer 17, no. 3 (2010) : 611-621.
http://dx.doi.org/10.1677/ERC-10-0016
---------- MLA ----------
Ahtiainen, P., Sharp, V., Rulli, S.B., Rivero-Müller, A., Mamaeva, V., Röyttä, M., et al. "Enhanced LH action in transgenic female mice expressing hCGβ-subunit induces pituitary prolactinomas; the role of high progesterone levels" . Endocrine-Related Cancer, vol. 17, no. 3, 2010, pp. 611-621.
http://dx.doi.org/10.1677/ERC-10-0016
---------- VANCOUVER ----------
Ahtiainen, P., Sharp, V., Rulli, S.B., Rivero-Müller, A., Mamaeva, V., Röyttä, M., et al. Enhanced LH action in transgenic female mice expressing hCGβ-subunit induces pituitary prolactinomas; the role of high progesterone levels. Endocr.-Relat. Cancer. 2010;17(3):611-621.
http://dx.doi.org/10.1677/ERC-10-0016