Fig. 7: A combination of p110α and EZH inhibitors induces regression of tumors with PIK3CA helical domain mutations, but not WT or kinase domain mutation.
From: Nuclear translocation of p85β promotes tumorigenesis of PIK3CA helical domain mutant cancer
a Subcutaneous xenograft tumors established from DLD1 cells were treated with vehicle or the indicated drugs. GSK2814126: an EZH2 inhibitor; Alpelisib: a p110α-specific inhibitor. b–g Tumors are treated with an EZH inhibitor Tazematostat (EPZ-6438), Alpelisib, or the drug combination. Subcutaneous xenograft tumors established from DLD1 parental cells (b), DLD1 PIK3CA E545K-only cells (c), DLD1 PIK3CA WT-only cells (d); a CRC patient-derived xenograft (PDX) with a PIK3CA H1047R kinase domain mutation (e), Vaco481 CRC cells with a PIK3CA Q546P mutation, or a CRC PDX with a PIK3CA E542K mutation (g). h Lysates of PIK3CA E542K mutant PDX tumors treated with the indicated drug were blotted with the indicated antibodies. Data from 10 tumors/group are presented as mean +SEM. Statistical analyses, two-way ANOVA. The Alpelisib data presented in (a) and (b) are the same dataset. Source data are provided as a Source Data file.
