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- W2356195641 abstract "Resistance against major endocrine therapy drug, tamoxifen, has been a serious issue in breast cancer treatment. A variety of data show that increased expression of epidermal growth factor receptor (EGFR),activation of the mitogen activated protein kinase (MAPK) and PI3K-Akt ( phosphatidylinositol-3-OH kinase) pathway are closely associated with endocrine resistance. Overexpression or loci mutation of HER-2 gene of about 15-30 percent of breast cancer patients is closely correlated with drug assistance and malignant prognosis. Increased growth factor signaling elements contribute to adaptive hypersensitivity in breast cancer cells by inter-play through genomic and non-genomic mechanism. The exquisitely low amounts of estrogen remanet after estrogen deprivation appear sufficient to allow development and maintenance of tumor cell growth. The common characteristics of acquired drug resistance after estrogen deprivation are overexpression of ERα, increased activity of the pathways of MAPK and PI3K.Increased growth factor signaling can also reduce ERα expression and/or function. Not surprisingly, the severe impact of elevated growth factor signaling on expression and function also resultes in estrogen independence and anti-estrogen resistance. Targeted growth factor receptor expression/activation, or key downstream signaling elements can effectively kill acquired-resistant cancer cells. Gefitinib can delay the drug resistance in breast cancer cells after estrogen elimination in vitro, and drastically inhibit proliferation of breast cancer cells resisting against tamoxifen simultaneously. Phase Ⅱ clinical trials demonstrate that R115777, a farnesyltransferase inhibitor, has a 24 percent efficacy in endocrine resistance breast cancer subjects. Preclinical studies show that CCI779, targeting to PI3K-Akt pathway, can eliminate ER+ resistance breast cancer cells. A variety of signaling pathways appear to constitute a highly integrated network rather than a simple linear structure down a single pathway. Thus, co-targeting therapy and broader target specificity are likely to be a better strategy than narrower targeting." @default.
- W2356195641 created "2016-06-24" @default.
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- W2356195641 date "2006-01-01" @default.
- W2356195641 modified "2023-09-24" @default.
- W2356195641 title "Research progress of growth factor pathway-driven endocrine resistance in breast cancer" @default.
- W2356195641 hasPublicationYear "2006" @default.
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