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breast, cancer, article, google, scholar, pubmed, cells, cas, receptor, cell, human, res, luminal, tumors, endocrine, stem, therapy, horwitz, estrogen, usa, research, cancers, expression, clin, oncol, cytokeratin, sartorius, tumor, access, resistance, privacy, cookies, content, positive, growth, molecular, natl, prognostic, university, colorado, medical, department, publish, search, steroid, negative, resistant, kabos, haughian, wang,

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month download article/chapter er−pr−ck5+ subpopulation found breast tumor-initiating cells majority er+pr+ck5− cells clinical oncology yia-pn200810-161 neoadjuvant endocrine therapy anti-er-targeted therapies tumorigenic breast-cancer cells node-positive breast cancer hormone receptor expression therapy resistant subpopulation tumor-initiating features er− tumor cells breast tumor xenografts full article pdf cd44+/cd24−/low cells anti-estrogens tamoxifen human breast carcinoma luminal breast cancers endocrine therapy residual breast cancers breast tumor heterogeneity breast cancer defined breast cancer subtypes recurrent breast cancer human breast tumours triple-negative phenotype luminal tumor xenografts cancer stem cells privacy choices/manage cookies neoplastic breast cells colorado cancer center primary breast cancers targeted therapies transforms primary breast cancer er+pr+ t47d steroid receptor negative triple-receptor measurements harvell dm progesterone receptor positive estrogen-receptor biology steroid receptor expression 5-bromo-2-deoxyuridine ck cheang mc creighton cj tumour stem cells luminal epithelial phenotype molecular profile subtype perou cm article kabos

Questions {❓}

• O’Brien CS, Howell SJ, Farnie G et al (2009) Resistance to endocrine therapy: are breast cancer stem cells the culprits?

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         headline:Cytokeratin 5 positive cells represent a steroid receptor negative and therapy resistant subpopulation in luminal breast cancers
         description:A majority of breast cancers are estrogen receptor (ER) positive and have a luminal epithelial phenotype. However, these ER+ tumors often contain heterogeneous subpopulations of ER− tumor cells. We previously identified a population of cytokeratin 5 (CK5) positive cells within ER+ and progesterone receptor positive (PR+) tumors that is both ER−PR− and CD44+, a marker of breast tumor-initiating cells (TICs). These CK5+ cells have properties of TICs in luminal tumor xenografts, and we speculated that they are more resistant to chemo- and anti-ER-targeted therapies than their ER+ neighbors. To test this, we used ER+PR+ T47D and MCF7 breast cancer cells. CK5+ cells had lower proliferative indices than CK5− cells, were less sensitive to 5-fluorouracil and docetaxel, and cultures became enriched for CK5+ cells after treatments. CK5+ cells were less prone to drug-induced apoptosis than CK5− cells. In cells treated with 17β-estradiol (E) plus anti-estrogens tamoxifen or fulvestrant, ER protein levels decreased, and CK5 protein levels increased, compared to controls treated with E alone. In ER+ tumors from patients treated with neoadjuvant endocrine therapies ER gene expression decreased, and CK5 gene expression increased in post compared to pre-treatment tumors. The number of CK5+ cells in tumors also increased in post- compared to pre-treatment tumors. We conclude that an ER−PR−CK5+ subpopulation found in many luminal tumors is resistant to standard endocrine and chemotherapies, relative to the majority ER+PR+CK5− cells. Compounds that effectively target these cells are needed to improve outcome in luminal breast cancers.
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      description:A majority of breast cancers are estrogen receptor (ER) positive and have a luminal epithelial phenotype. However, these ER+ tumors often contain heterogeneous subpopulations of ER− tumor cells. We previously identified a population of cytokeratin 5 (CK5) positive cells within ER+ and progesterone receptor positive (PR+) tumors that is both ER−PR− and CD44+, a marker of breast tumor-initiating cells (TICs). These CK5+ cells have properties of TICs in luminal tumor xenografts, and we speculated that they are more resistant to chemo- and anti-ER-targeted therapies than their ER+ neighbors. To test this, we used ER+PR+ T47D and MCF7 breast cancer cells. CK5+ cells had lower proliferative indices than CK5− cells, were less sensitive to 5-fluorouracil and docetaxel, and cultures became enriched for CK5+ cells after treatments. CK5+ cells were less prone to drug-induced apoptosis than CK5− cells. In cells treated with 17β-estradiol (E) plus anti-estrogens tamoxifen or fulvestrant, ER protein levels decreased, and CK5 protein levels increased, compared to controls treated with E alone. In ER+ tumors from patients treated with neoadjuvant endocrine therapies ER gene expression decreased, and CK5 gene expression increased in post compared to pre-treatment tumors. The number of CK5+ cells in tumors also increased in post- compared to pre-treatment tumors. We conclude that an ER−PR−CK5+ subpopulation found in many luminal tumors is resistant to standard endocrine and chemotherapies, relative to the majority ER+PR+CK5− cells. Compounds that effectively target these cells are needed to improve outcome in luminal breast cancers.
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         Endocrine therapy
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         Breast cancer
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