Artículo

Wargon, V.; Helguero, L.A.; Bolado, J.; Rojas, P.; Novaro, V.; Molinolo, A.; Lanari, C. "Reversal of antiprogestin resistance and progesterone receptor isoform ratio in acquired resistant mammary carcinomas" (2009) Breast Cancer Research and Treatment. 116(3):449-460
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Abstract:

To explore mechanisms related to hormone resistance, three resistant variants of the MPA mouse breast cancer tumor model with low levels of progesterone receptor (PR) isoform A (PR-A)/high PR-B expression were developed by prolonged selective pressure with antiprogestins. The resistant phenotype of one tumor line was reversed spontaneously after several consecutive passages in syngeneic BALB/c mice or by 17-b-estradiol or tamoxifen treatment, and this reversion was significantly associated with an increase in PR-A expression. The responsive parental tumors disclosed low activation of ERK and high activation of AKT; resistant tumors on the other hand, showed the opposite, and this was associated with a higher metastatic potential, that did not revert. This study shows for the first time in vivo a relationship between PR isoform expression and antiprogestin responsiveness, demonstrating that, whereas acquired resistance may be reversed, changes in kinase activation and metastatic potential are unidirectional associated with tumor progression. © Springer Science+Business Media, LLC. 2008.

Registro:

Documento: Artículo
Título:Reversal of antiprogestin resistance and progesterone receptor isoform ratio in acquired resistant mammary carcinomas
Autor:Wargon, V.; Helguero, L.A.; Bolado, J.; Rojas, P.; Novaro, V.; Molinolo, A.; Lanari, C.
Filiación:Laboratory of Hormonal Carcinogenesis, Institute of Experimental Biology and Medicine (IBYME), National Research Council of Argentina (CONICET), Obligado 2490, 1428 Buenos Aires, Argentina
Department of Biosciences and Nutrition, Karolinska Institutet, 141 57 Stockholm, Sweden
Oral and Pharyngeal Cancer Branch, NIDCR, NIH, Bethesda, MD 20892-4340, United States
Palabras clave:Acquired hormone resistance; AKT; Antiprogestins; Breast cancer; De novo hormone resistance; ERK; Estrogen receptors; Hormone resistance; Metastasis; Progesterone receptor isoforms; Tumor regression; estradiol; estrogen receptor alpha; lonaprisan; mifepristone; mitogen activated protein kinase 1; mitogen activated protein kinase 3; progesterone receptor A; progesterone receptor B; protein kinase B; tamoxifen; hormone antagonist; isoprotein; mifepristone; mitogen activated protein kinase 1; mitogen activated protein kinase 3; progesterone receptor; progesterone receptor A; progesterone receptor B; protein kinase B; animal experiment; animal model; animal tissue; article; axillary lymph node; breast cancer; breast carcinoma; cancer inhibition; cancer resistance; controlled study; female; lymph node metastasis; metastasis potential; mouse; nonhuman; priority journal; tumor growth; animal; Bagg albino mouse; cell proliferation; drug resistance; experimental neoplasm; fluorescent antibody technique; metabolism; pathology; survival rate; Western blotting; Animals; Blotting, Western; Cell Proliferation; Drug Resistance, Neoplasm; Female; Fluorescent Antibody Technique; Hormone Antagonists; Lymphatic Metastasis; Mammary Neoplasms, Experimental; Mice; Mice, Inbred BALB C; Mifepristone; Mitogen-Activated Protein Kinase 1; Mitogen-Activated Protein Kinase 3; Protein Isoforms; Proto-Oncogene Proteins c-akt; Receptors, Progesterone; Survival Rate
Año:2009
Volumen:116
Número:3
Página de inicio:449
Página de fin:460
DOI: http://dx.doi.org/10.1007/s10549-008-0150-y
Título revista:Breast Cancer Research and Treatment
Título revista abreviado:Breast Cancer Res. Treat.
ISSN:01676806
CODEN:BCTRD
CAS:estradiol, 50-28-2; lonaprisan, 211254-73-8; mifepristone, 84371-65-3; mitogen activated protein kinase 1, 137632-08-7; mitogen activated protein kinase 3, 137632-07-6; protein kinase B, 148640-14-6; tamoxifen, 10540-29-1; Hormone Antagonists; Mifepristone, 84371-65-3; Mitogen-Activated Protein Kinase 1, 2.7.1.37; Mitogen-Activated Protein Kinase 3, 2.7.1.37; Protein Isoforms; Proto-Oncogene Proteins c-akt, 2.7.1.37; Receptors, Progesterone; progesterone receptor A; progesterone receptor B
Registro:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_01676806_v116_n3_p449_Wargon

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Citas:

---------- APA ----------
Wargon, V., Helguero, L.A., Bolado, J., Rojas, P., Novaro, V., Molinolo, A. & Lanari, C. (2009) . Reversal of antiprogestin resistance and progesterone receptor isoform ratio in acquired resistant mammary carcinomas. Breast Cancer Research and Treatment, 116(3), 449-460.
http://dx.doi.org/10.1007/s10549-008-0150-y
---------- CHICAGO ----------
Wargon, V., Helguero, L.A., Bolado, J., Rojas, P., Novaro, V., Molinolo, A., et al. "Reversal of antiprogestin resistance and progesterone receptor isoform ratio in acquired resistant mammary carcinomas" . Breast Cancer Research and Treatment 116, no. 3 (2009) : 449-460.
http://dx.doi.org/10.1007/s10549-008-0150-y
---------- MLA ----------
Wargon, V., Helguero, L.A., Bolado, J., Rojas, P., Novaro, V., Molinolo, A., et al. "Reversal of antiprogestin resistance and progesterone receptor isoform ratio in acquired resistant mammary carcinomas" . Breast Cancer Research and Treatment, vol. 116, no. 3, 2009, pp. 449-460.
http://dx.doi.org/10.1007/s10549-008-0150-y
---------- VANCOUVER ----------
Wargon, V., Helguero, L.A., Bolado, J., Rojas, P., Novaro, V., Molinolo, A., et al. Reversal of antiprogestin resistance and progesterone receptor isoform ratio in acquired resistant mammary carcinomas. Breast Cancer Res. Treat. 2009;116(3):449-460.
http://dx.doi.org/10.1007/s10549-008-0150-y