BRCA1-IRIS inactivation overcomes paclitaxel resistance in triple negative breast cancers

Conclusions:
In addition to driving TNBC tumor formation, BRCA1-IRIS overexpression drives their intrinsic and acquired paclitaxel resistance, partly by activating autocrine signaling loops EGF/EGFR-ErbB2 and NRG1/ErbB2-ErbB3. These loops activate AKT, causing FOXO3a degradation and survivin overexpression. Taken together, this underscores the need for BRCA1-IRIS specific therapy and strongly suggests that BRCA1-IRIS and/or signaling loops activated by it could be rational therapeutic targets for advanced TNBCs.

Source: Breast Cancer Research - January 13, 2015 Category: Cancer & Oncology Authors: Zannel BlanchardBibbin PaulBarbara CraftWael ElShamy Source Type: research