Bcl-w is a pericyte-induced antiapoptotic protein in ECs. (A-B) Expression of Bcl-w in ECs (A) or OCs (B) comprising cancer cells, pericytes, macrophages, and infrequent cancer-associated fibroblastic cells fractionated from PNET tumors excised from RIP1-Tag2 mice that had been treated with control or imatinib, as assessed by quantitative RT-PCR (n = 10 in each group, data shown are representative for 2 independent EC isolations). **P < .01 vs control, Student t test. (C) Immunostaining of sections from PNET of RIP1-Tag2 mice or B16/PDGFB tumors for Bcl-w (red) and CD31 (green). Cell nuclei (DAPI), blue. Original magnification, 200× (for high magnification image, 630×). The panels are representative of at least 5 fields in 5 tissue sections taken from 5 mice. (D) Number of MS1 pancreatic islet ECs after siRNA-mediated knockdown of Bcl-w and treatment with control or vinblastine (50 ng/mL). A nontargeting siRNA was used as a control. Data shown are representative for 3 independent experiments. **P < .01 vs nontargeting/vinblastine, Student t test. (E) Expression of Bcl-w in isolated ECs from B16/mock and B16/PDGFB tumors assessed by quantitative RT-PCR (n = 4 in each group, data shown are representative for 2 independent EC isolations). *P < .05 vs B16/mock, Student t test.