Title : Tamoxifen resistance in breast tumors is driven by growth factor receptor signaling with repression of classic estrogen receptor genomic function.

Pub. Date : 2008 Feb 1

PMID : 18245484






5 Functional Relationships(s)
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Compound Name
Protein Name
Organism
1 Epidermal growth factor receptor (EGFR) and HER2, which were barely detected in control estrogen-treated tumors, increased slightly with tamoxifen and were markedly increased when tumors became resistant. Tamoxifen epidermal growth factor receptor Homo sapiens
2 Epidermal growth factor receptor (EGFR) and HER2, which were barely detected in control estrogen-treated tumors, increased slightly with tamoxifen and were markedly increased when tumors became resistant. Tamoxifen epidermal growth factor receptor Homo sapiens
3 Phosphorylated levels of p42/44 and p38 mitogen-activated protein kinases (both downstream of EGFR/HER2) were increased in the tamoxifen-resistant tumors and were suppressed by gefitinib. Tamoxifen epidermal growth factor receptor Homo sapiens
4 Phosphorylated insulin-like growth factor-IR (IGF-IR), which can interact with both EGFR and membrane ER, was elevated in the tamoxifen-resistant tumors compared with the sensitive group. Tamoxifen epidermal growth factor receptor Homo sapiens
5 In conclusion, EGFR/HER2 may mediate tamoxifen resistance in ER-positive breast cancer despite continued suppression of ER genomic function by tamoxifen. Tamoxifen epidermal growth factor receptor Homo sapiens