Crosstalk between the estrogen receptor and the HER tyrosine kinase receptor family: molecular mechanism and clinical implications for endocrine therapy resistance. Export

@article{citeulike:3467737, abstract = {Breast cancer evolution and tumor progression are governed by the complex interactions between steroid receptor [estrogen receptor (ER) and progesterone receptor] and growth factor receptor signaling. In recent years, the field of cancer therapy has witnessed the emergence of multiple strategies targeting these specific cancer pathways and key molecules (ER and growth factor receptors) to arrest tumor growth and achieve tumor eradication; treatment success, however, has varied and both de novo (up front) and acquired resistance have proven a challenge. Recent studies of ER biology have revealed new insights into ER action in breast cancer and have highlighted the role of an intimate crosstalk between the ER and HER family signaling pathways as a fundamental contributor to the development of resistance to endocrine therapies against the ER pathway. The aim of this review article is to summarize the current knowledge on mechanisms of resistance of breast cancer cells to endocrine therapies due to the crosstalk between the ER and the HER growth factor receptor signaling pathways and to explore new available therapeutic strategies that could prolong duration of response and circumvent endocrine resistant tumor growth.}, author = {Arpino, Grazia and Wiechmann, Lisa and Osborne, C. Kent and Schiff, Rachel}, citeulike-article-id = {3467737}, citeulike-linkout-0 = {http://dx.doi.org/10.1210/er.2006-0045}, citeulike-linkout-1 = {http://edrv.endojournals.org/cgi/content/abstract/29/2/217}, citeulike-linkout-2 = {http://view.ncbi.nlm.nih.gov/pubmed/18216219}, citeulike-linkout-3 = {http://www.hubmed.org/display.cgi?uids=18216219}, day = {1}, doi = {10.1210/er.2006-0045}, issn = {0163-769X}, journal = {Endocrine reviews}, keywords = {er, era, era\_target, mapk, pathway, pi3k, rac, raf, ras, review}, month = {April}, number = {2}, pages = {217--233}, posted-at = {2009-09-28 19:30:30}, priority = {2}, title = {Crosstalk between the estrogen receptor and the HER tyrosine kinase receptor family: molecular mechanism and clinical implications for endocrine therapy resistance.}, url = {http://dx.doi.org/10.1210/er.2006-0045}, volume = {29}, year = {2008} }

TY - JOUR ID - citeulike:3467737 L3 - citeulike-article-id:3467737 N2 - Breast cancer evolution and tumor progression are governed by the complex interactions between steroid receptor [estrogen receptor (ER) and progesterone receptor] and growth factor receptor signaling. In recent years, the field of cancer therapy has witnessed the emergence of multiple strategies targeting these specific cancer pathways and key molecules (ER and growth factor receptors) to arrest tumor growth and achieve tumor eradication; treatment success, however, has varied and both de novo (up front) and acquired resistance have proven a challenge. Recent studies of ER biology have revealed new insights into ER action in breast cancer and have highlighted the role of an intimate crosstalk between the ER and HER family signaling pathways as a fundamental contributor to the development of resistance to endocrine therapies against the ER pathway. The aim of this review article is to summarize the current knowledge on mechanisms of resistance of breast cancer cells to endocrine therapies due to the crosstalk between the ER and the HER growth factor receptor signaling pathways and to explore new available therapeutic strategies that could prolong duration of response and circumvent endocrine resistant tumor growth. IS - 2 JF - Endocrine reviews SN - 0163-769X EP - 233 TI - Crosstalk between the estrogen receptor and the HER tyrosine kinase receptor family: molecular mechanism and clinical implications for endocrine therapy resistance. VL - 29 SP - 217 KW - er KW - era KW - era_target KW - mapk KW - pathway KW - pi3k KW - rac KW - raf KW - ras KW - review AU - Arpino, Grazia AU - Wiechmann, Lisa AU - Osborne, Kent AU - Schiff, Rachel PY - 2008/04/01/ UR - http://dx.doi.org/10.1210/er.2006-0045 ER -