Does bRCA1-IRIS inactivation overcome paclitaxel resistance in triple negative breast cancers?
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.
The frequency of unhealthy snack consumption decreased from 2001 to 2008 in schoolchildren in Norway. The decrease was most evident among children at schools participating in the national free school fruit program and in children with a low socioeconomic status.