The DOI matches its Crossref record; 47 of the 47 references it cites were found in a registry or an index.
Molecular Changes in Tamoxifen-Resistant Breast Cancer: Relationship Between Estrogen Receptor, HER-2, and p38 Mitogen-Activated Protein Kinase
Open accessAbstract
Purpose: To evaluate growth factor receptor cross talk with the estrogen receptor (ER) in paired clinical breast cancer specimens and in a xenograft model before tamoxifen and at tumor progression as a possible mechanism for tamoxifen resistance. Methods: Specimen pairs from 39 patients were tissue arrayed and stained for ER, progesterone receptor (PgR), Bcl-2, c-ErbB2 (HER-2), and phosphorylated (p) p38 mitogen-activated protein kinase (MAPK), p-ERK1/2 MAPK, and p-Akt. Xenograft MCF-7 tumors before and after tamoxifen resistance were assessed for levels of p-p38. Results: Pretreatment, there were strong correlations between ER, PgR, and Bcl-2, and an inverse correlation between ER and HER-2. These correlations were lost in the tamoxifen- resistant tumors and replaced by strong correlations between ER and p-p38 and p-ERK. ER expression was lost in 17% of resistant tumors. Three (11%) of the 26 tumors originally negative for HER-2 became amplified and/or overexpressed at resistance. All ER-positive tumors that overexpressed HER-2 originally or at resistance expressed high levels of p-p38. In the pretreatment and tamoxifen-resistant specimens, there were strong correlations between p-p38 and p-ERK. In the tamoxifen-resistant xenograft tumors, like the clinical samples, there was a striking increase in p-p38. Conclusion: The molecular pathways driving tumor growth can change as the tumor progresses. Crosstalk between ER, HER-2, p38, and ERK may contribute to tamoxifen resistance and may provide molecular targets to overcome this resistance.
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Self-citationActivation of the estrogen receptor through phosphorylation by mitogen-activated protein kinase
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AIB1, a Steroid Receptor Coactivator Amplified in Breast and Ovarian Cancer
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Self-citationPhosphatidylinositol 3-Kinase/AKT-mediated Activation of Estrogen Receptor α
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Biological determinants of endocrine resistance in breast cancer
Musgrove, E. A., & Sutherland, R. L. (2009) · Nature Reviews Cancer · doi:10.1038/nrc2713 · Cited by 1,252
ESR1 ligand-binding domain mutations in hormone-resistant breast cancer
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Self-citationPatel, H. K., & Bihani, T. (2018) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2017.12.012 · Cited by 499
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Metadata
- Authors
- Gutierrez, M. C., Detre, S., Johnston, S., Mohsin, S. K., Shou, J., Allred, D. C., Schiff, R., Osborne, C. K., & Dowsett, M.
- Venue
- Journal of Clinical Oncology
- Published
- 2005-04-10
- Volume
- 23
- Issue
- 11
- Pages
- 2469-2476
- ISSN
- 0732-183X (ISSN-L)
- 1527-7755
- OpenAlex
- W2137355132
- Cited by
- 489
- References
- 47
- FWCI
- 16.30
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Gutierrez, M. C., Detre, S., Johnston, S., Mohsin, S. K., Shou, J., Allred, D. C., Schiff, R., Osborne, C. K., & Dowsett, M. (2005). Molecular Changes in Tamoxifen-Resistant Breast Cancer: Relationship Between Estrogen Receptor, HER-2, and p38 Mitogen-Activated Protein Kinase. Journal of Clinical Oncology. https://doi.org/10.1200/jco.2005.01.172
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