Title : Bruton's Tyrosine Kinase Inhibitors Prevent Therapeutic Escape in Breast Cancer Cells.

Pub. Date : 2016 Sep

PMID : 27256378






7 Functional Relationships(s)
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1 Ibrutinib treatment impacts HER2(+) breast cancer cell viability at lower concentrations than the established breast cancer therapeutic lapatinib. ibrutinib erb-b2 receptor tyrosine kinase 2 Homo sapiens
2 In addition to inhibiting BTK, ibrutinib, but not AVL-292 and CGI-1746, efficiently blocks the activation of EGFR, HER2, ErbB3, and ErbB4. ibrutinib erb-b2 receptor tyrosine kinase 2 Homo sapiens
3 HER2(+) breast cancer cell proliferation is blocked by ibrutinib even in the presence of these factors. ibrutinib erb-b2 receptor tyrosine kinase 2 Homo sapiens
4 In vivo, ibrutinib inhibits HER2(+) xenograft tumor growth. ibrutinib erb-b2 receptor tyrosine kinase 2 Homo sapiens
5 Consistent with this, immunofluorescence analysis of xenograft tumors shows that ibrutinib reduces the phosphorylation of HER2, BTK, Akt, and Erk and histone H3 and increases cleaved caspase-3 signals. ibrutinib erb-b2 receptor tyrosine kinase 2 Homo sapiens
6 As BTK-C and HER2 are often coexpressed in human breast cancers, these observations indicate that BTK-C is a potential therapeutic target and that ibrutinib could be an effective drug especially for HER2(+) breast cancer. ibrutinib erb-b2 receptor tyrosine kinase 2 Homo sapiens
7 As BTK-C and HER2 are often coexpressed in human breast cancers, these observations indicate that BTK-C is a potential therapeutic target and that ibrutinib could be an effective drug especially for HER2(+) breast cancer. ibrutinib erb-b2 receptor tyrosine kinase 2 Homo sapiens