scholarly journals Human breast cancer cells generated by oncogenic transformation of primary mammary epithelial cells

2001 ◽  
Vol 15 (1) ◽  
pp. 50-65 ◽  
Author(s):  
B. Elenbaas
Keyword(s):  
Breast Cancer ◽  
Epithelial Cells ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Human Breast Cancer Cells ◽  
Oncogenic Transformation ◽  
Human Breast

scholarly journals Benign mammary epithelial cells enhance the transformed phenotype of human breast cancer cells

BMC Cancer ◽  
2010 ◽  
Vol 10 (1) ◽  
Author(s):  
Joanna M Poczobutt ◽  
John Tentler ◽  
Xian Lu ◽  
Pepper J Schedin ◽  
Arthur Gutierrez-Hartmann
Keyword(s):  
Breast Cancer ◽  
Epithelial Cells ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Human Breast Cancer Cells ◽  
Human Breast

scholarly journals Proliferation of Endothelial and Tumor Epithelial Cells by Progestin-Induced Vascular Endothelial Growth Factor from Human Breast Cancer Cells: Paracrine and Autocrine Effects

Endocrinology ◽  
2005 ◽  
Vol 146 (8) ◽  
pp. 3632-3641 ◽  
Author(s):  
Yayun Liang ◽  
Salman M. Hyder
Keyword(s):  
Breast Cancer ◽  
Epithelial Cells ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Vascular Endothelial ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Angiogenic Growth Factors ◽  
Endothelial Growth Factor

Abstract Angiogenesis, the formation of new blood vessels, is essential for tumor expansion, and vascular endothelial growth factor (VEGF) is one of the most potent angiogenic growth factors known. We have previously shown that natural and synthetic progestins, including those used in hormone replacement therapy and oral contraception, induce the synthesis and secretion of VEGF in a subset of human breast cancer cells in a progesterone receptor-dependent manner. We now report that conditioned medium from progestin-treated breast tumor cells can induce the proliferation of endothelial cells in a paracrine manner and induce the proliferation of tumor epithelial cells in a paracrine and an autocrine manner. The use of an anti-VEGF antibody and SU-1498, an inhibitor of VEGF receptor-2 (VEGFR-2 or flk/kdr) tyrosine kinase activity, demonstrated that these effects involve interactions between VEGF and VEGFR-2. Also, blockage of progestin-induced VEGF by the antiprogestin RU-486 (mifepristone) eliminated VEGF-induced proliferative effects. The ability of VEGF to increase the proliferation of endothelial cells and tumor cells, including those that do not release VEGF in response to progestins, suggests that these effects are mediated by amplification of the progestin signal, which culminates in angiogenesis and tumor growth. These novel findings suggest that targeting the release of VEGF from tumor epithelial cells as well as blocking interactions between VEGF and VEGFR-2 on both endothelial and tumor epithelial cells may facilitate the development of new antiangiogenic therapies for progestin-dependent breast tumors. Furthermore, these data indicate that it would be useful to develop selective progesterone receptor modulators that prevent the release of angiogenic growth factors from breast cancer cells.

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