4.5 Article

Reversal of antiprogestin resistance and progesterone receptor isoform ratio in acquired resistant mammary carcinomas

期刊

BREAST CANCER RESEARCH AND TREATMENT
卷 116, 期 3, 页码 449-460

出版社

SPRINGER
DOI: 10.1007/s10549-008-0150-y

关键词

Acquired hormone resistance; AKT; Antiprogestins; Breast cancer; De novo hormone resistance; ERK; Estrogen receptors; Hormone resistance; Metastasis; Progesterone receptor isoforms; Tumor regression

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资金

  1. Sales Foundation, SECyT [PICT 03-14406, PICT 05-15038]
  2. CONICET [PIP 5351]

向作者/读者索取更多资源

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-beta-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.

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