Role of the estrogen receptor coactivator AIB1 (SRC-3) and HER-2/neu in tamoxifen resistance in breast cancer.
By C. Osborne, V. Bardou, Torsten A. Hopp, G. Chamness, S. Hilsenbeck, S. Fuqua, J. Wong, D. Allred, G. Clark, R. Schiff. Journal of the National Cancer Institute, 2003
831 citations recorded by the source corpus.
Subfields: Cancer Research, Genetics, Oncology
View Paper: https://www.semanticscholar.org/paper/3c54de583f5573219db58637ed486972272d38cc
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Citations in the corpus
- Overcoming Endocrine Resistance in Breast Cancer (2020, positive): “For instance, overexpression of SRCs results in a switch of the antagonistic activity of tamoxifen-bound ER to an agonistic role (Osborne et al., 2003).”
- Coregulator function: a key to understanding tissue specificity of selective receptor modulators. (2004, neutral): “which is indicative of tamoxifen resistance (302).”
- Mechanisms of tamoxifen resistance: increased estrogen receptor-HER2/neu cross-talk in ER/HER2-positive breast cancer. (2004, background): “We have previously reported that ER-positive human breast cancers that overexpress AIB1, especially those that also overexpress HER2, are resistant to adjuvant therapy with tamoxifen ( 11 ).”
- Biological determinants of endocrine resistance in breast cancer (2009, background): “and is associated with reduced responsiveness to tamoxifen in patient”
- Mechanisms of tamoxifen resistance. (2004, methodology): “There is clinical evidence to support this hypothesis (Osborne et al. 2003).”
- Meeting highlights: updated international expert consensus on the primary therapy of early breast cancer. (2003, background): “Estrogen and progesterone receptor content in the primary tumor are powerful markers to predict endocrine responsiveness in their presence(74) and cytotoxic responsiveness in their absence.(15,19,20,51,75-77) This does not mean that patients with tumors expressing hormone receptors do not benefit fr”
- The different roles of ER subtypes in cancer biology and therapy (2011, background): “The cytoplasmic localization of proline, glutamate and leucine-rich protein 1 (PELP1) and the expression of the truncated ERα variant ERα-36 have been reported to promote constitutive ERα-mediated transcription, which also decreases sensitivity in vitro and is associated with reduced responsivenes”