We are analyzing https://link.springer.com/article/10.1007/s10911-009-9115-y.

Title:
Resistance to Endocrine Therapy: Are Breast Cancer Stem Cells the Culprits? | Journal of Mammary Gland Biology and Neoplasia
Description:
From a developmental point of view, tumors can be seen as aberrant versions of their tissue of origin. For example, tumors often partially retain differentiation markers of their tissue of origin and there is evidence that they contain cancer stem cells (CSCs) that drive tumorigenesis. In this review, we summarise current evidence that breast CSCs may partly explain endocrine resistance in breast cancer. In normal breast, the stem cells are known to possess a basal phenotype and to be mainly ERα−. If the hierarchy in breast cancer reflects this, the breast CSC may be endocrine resistant because it expresses very little ERα and can only respond to treatment by virtue of paracrine influences of neighboring, differentiated ERα+ tumor cells. Normal breast epithelial stem cells are highly dependent on the EGFR and other growth factor receptors and it may be that the observed increased growth factor receptor expression in endocrine-resistant breast cancers reflects an increased proportion of CSCs selected by endocrine therapies. There is evidence from a number of studies that breast CSCs are ERα− and EGFR+/HER2+, which would support this view. CSCs also express mesenchymal genes which are suppressed by ERα expression, further indicating the mutual exclusion between ERα+ cells and the CSCs. As we learn more about CSCs, differentiation and the expression and functional activity of the ERα in these cells in diverse breast tumor sub-types, it is hoped that our understanding will lead to new modalities to overcome the problem of endocrine resistance in the clinic.
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Keywords {🔍}

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Topics {✒️}

human colon-cancer-initiating cells phosphatidylinositol 3-kinase/akt-mediated activation month download article/chapter stem/progenitor cell properties 2/neu-positive breast cancer er-nfĸb-driven stem tamoxifen-resistant mcf-7 cells epidermal growth factor endothelium-tumour cell interactions breast csc negative predictive factor cancer stem cells estrogen receptor-positive breast cancer cells human breast cancer breast carcinoma cells c-met receptor estrogen receptor gene epithelial progesterone receptor human brain tumors full article pdf breast cancer reflects estrogen receptor alpha estrogen receptor-alpha cancer stem cell growth factor receptors initiating tumour growth anti-estrogen resistance primary breast cancer oestrogen receptor alpha human breast tumours tumor-initiating cells child mammary tissue single stem cell enhances cellular migration histone deacetylase inhibitor steroid receptor expression cell stem cell tumour–stroma interactions postmenopausal breast cancer breast cancer progression breast cancer suggests breast cancer subtypes breast cancer packs breast cancer patients advanced breast cancer progesterone receptor status estrogen receptor expression privacy choices/manage cookies breast cancer res

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Resistance to Endocrine Therapy: Are Breast Cancer Stem Cells the Culprits?
Resistance to Endocrine Therapy: Are Breast Cancer Stem Cells the Culprits?

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      description:From a developmental point of view, tumors can be seen as aberrant versions of their tissue of origin. For example, tumors often partially retain differentiation markers of their tissue of origin and there is evidence that they contain cancer stem cells (CSCs) that drive tumorigenesis. In this review, we summarise current evidence that breast CSCs may partly explain endocrine resistance in breast cancer. In normal breast, the stem cells are known to possess a basal phenotype and to be mainly ERα−. If the hierarchy in breast cancer reflects this, the breast CSC may be endocrine resistant because it expresses very little ERα and can only respond to treatment by virtue of paracrine influences of neighboring, differentiated ERα+ tumor cells. Normal breast epithelial stem cells are highly dependent on the EGFR and other growth factor receptors and it may be that the observed increased growth factor receptor expression in endocrine-resistant breast cancers reflects an increased proportion of CSCs selected by endocrine therapies. There is evidence from a number of studies that breast CSCs are ERα− and EGFR+/HER2+, which would support this view. CSCs also express mesenchymal genes which are suppressed by ERα expression, further indicating the mutual exclusion between ERα+ cells and the CSCs. As we learn more about CSCs, differentiation and the expression and functional activity of the ERα in these cells in diverse breast tumor sub-types, it is hoped that our understanding will lead to new modalities to overcome the problem of endocrine resistance in the clinic.
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