We are analyzing https://link.springer.com/article/10.1023/a:1024031731269.

Title:
Progesterone Receptors A and B Differentially Affect the Growth of Estrogen-Dependent Human Breast Tumor Xenografts | Breast Cancer Research and Treatment
Description:
Sixty to seventy percent of all primary human breast cancers are estrogen-dependent and express both estrogen (ER) and progesterone receptors (PR). Whereas expression of the two naturally occurring PR isoforms, PR-A and PR-B, is close to equimolar in normal human tissues, the ratio of the two receptors varies extensively in tumors. This is important since the two PR are functionally distinct and have differential repressor effects on ER. The PR isoform content may, therefore, affect the outcome of endocrine therapies targeted at ER. Study of PR isoforms is difficult because the two receptors are co-expressed in cells under estradiol stimulation. We have engineered four sets of T47D human breast cancer cells that, independent of estrogen: (i) express only PR-A; (ii) express only PR-B; (iii) are PR-negative; or (iv) contain both PR isoforms. Each of these cell lines was grown into solid tumors in nude mice in a strictly 17β-estradiol-dependent manner. Results show, first, that PR-A expressing cells grow into tumors that are approximately half the size of PR-B expressing tumors, and second, that the reduced growth of PR-A tumors occurs in the absence of PR ligand. Tamoxifen treatment preferentially inhibited the growth of PR-A tumors, whereas PR-B tumors were unaffected. Thus, PR are not just passive markers of functional ER; the prevalence of PR-A or PR-B may differentially influence tumor phenotype.
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Keywords {🔍}

breast, google, scholar, cancer, progesterone, human, receptor, receptors, horwitz, article, cell, estrogen, isoforms, cells, res, biol, growth, pra, tumors, access, characterization, chem, content, sartorius, expression, prb, mol, privacy, cookies, function, research, tumor, mice, hormone, endocrinol, usa, steroid, information, publish, search, affect, xenografts, shen, cancers, differential, study, open, tung, takimoto, regulation,

Topics {✒️}

strictly 17β-estradiol-dependent manner hormone-dependent breast cancers month download article/chapter improved relapse-free survival antiprogestin-occupied b-receptors high progesterone-receptor levels progesterone receptor-mediated transcription unique n-terminal segment single steroid-binding subunit cyclin-dependent kinase inhibitors endocrine therapies targeted steroid hormone receptors human breast cancer small breast carcinomas human progesterone receptor human estrogen receptor related subjects specific progesterone receptors clinicopathologic tumor parameters primary breast cancer estrogen receptors alpha privacy choices/manage cookies full article pdf rabbit progesterone receptor unoccupied progesterone receptor receptors varies extensively oestrogen receptor-α ligand binding specificity malignant breast disease progesterone receptor isoforms differential repressor effects receptor signaling pathways estrogen receptor beta expressing cells grow hormonal prevention tumorigenic cell lines ligand-independent activation promoter-specific repressor normal human tissues differential cofactor binding european economic area limiting factor mediates transcript tissue distribution responses illustrate interactions o'malley bw induce sexual behavior van golen kl differential gene regulation check access instant access

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      headline:Progesterone Receptors A and B Differentially Affect the Growth of Estrogen-Dependent Human Breast Tumor Xenografts
      description:Sixty to seventy percent of all primary human breast cancers are estrogen-dependent and express both estrogen (ER) and progesterone receptors (PR). Whereas expression of the two naturally occurring PR isoforms, PR-A and PR-B, is close to equimolar in normal human tissues, the ratio of the two receptors varies extensively in tumors. This is important since the two PR are functionally distinct and have differential repressor effects on ER. The PR isoform content may, therefore, affect the outcome of endocrine therapies targeted at ER. Study of PR isoforms is difficult because the two receptors are co-expressed in cells under estradiol stimulation. We have engineered four sets of T47D human breast cancer cells that, independent of estrogen: (i) express only PR-A; (ii) express only PR-B; (iii) are PR-negative; or (iv) contain both PR isoforms. Each of these cell lines was grown into solid tumors in nude mice in a strictly 17β-estradiol-dependent manner. Results show, first, that PR-A expressing cells grow into tumors that are approximately half the size of PR-B expressing tumors, and second, that the reduced growth of PR-A tumors occurs in the absence of PR ligand. Tamoxifen treatment preferentially inhibited the growth of PR-A tumors, whereas PR-B tumors were unaffected. Thus, PR are not just passive markers of functional ER; the prevalence of PR-A or PR-B may differentially influence tumor phenotype.
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