Reversal of antiprogestin resistance and progesterone receptor isoform ratio in acquired resistant mammary carcinomas
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...
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2009
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| LEADER | 20816caa a22019937a 4500 | ||
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| 001 | PAPER-23121 | ||
| 003 | AR-BaUEN | ||
| 005 | 20230518205446.0 | ||
| 008 | 190411s2009 xx ||||fo|||| 00| 0 eng|d | ||
| 024 | 7 | |2 scopus |a 2-s2.0-70349577376 | |
| 024 | 7 | |2 cas |a 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 | |
| 040 | |a Scopus |b spa |c AR-BaUEN |d AR-BaUEN | ||
| 030 | |a BCTRD | ||
| 100 | 1 | |a Wargon, V. | |
| 245 | 1 | 0 | |a Reversal of antiprogestin resistance and progesterone receptor isoform ratio in acquired resistant mammary carcinomas |
| 260 | |c 2009 | ||
| 270 | 1 | 0 | |m Lanari, C.; Laboratory of Hormonal Carcinogenesis, Institute of Experimental Biology and Medicine (IBYME), National Research Council of Argentina (CONICET), Obligado 2490, 1428 Buenos Aires, Argentina; email: clanari@dna.uba.ar |
| 506 | |2 openaire |e Política editorial | ||
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| 520 | 3 | |a 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. |l eng | |
| 536 | |a Detalles de la financiación: Secretaria de Ciencia y Tecnica, Universidad de Buenos Aires, PICT 05-15038, PICT 03-14406 | ||
| 536 | |a Detalles de la financiación: Consejo Nacional de Investigaciones Científicas y Técnicas, PIP 5351 | ||
| 536 | |a Detalles de la financiación: Financial support Sales Foundation, SECyT (PICT 03-14406 and PICT 05-15038) and CONICET (PIP 5351). | ||
| 593 | |a Laboratory of Hormonal Carcinogenesis, Institute of Experimental Biology and Medicine (IBYME), National Research Council of Argentina (CONICET), Obligado 2490, 1428 Buenos Aires, Argentina | ||
| 593 | |a Department of Biosciences and Nutrition, Karolinska Institutet, 141 57 Stockholm, Sweden | ||
| 593 | |a Oral and Pharyngeal Cancer Branch, NIDCR, NIH, Bethesda, MD 20892-4340, United States | ||
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