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• W1967687440 abstract "Durable responses to imatinib monotherapy are rarely seen in aggressive forms of Philadelphia chromosome positive (Ph+) leukemias. To investigate the possible cause of treatment failure we examined the role of protein kinase C epsilon (PKCE), an oncogene highly implicated in the development of solid tumors and resistance to chemotherapy. We found high levels of PKCE transcripts in Ph+ acute lymphoblastic leukemia (ALL) cells from patients and cell lines, and imatinib resistant chronic myeloid leukemia, which were also less responsive to imatinib-induced apoptosis than Ph+ cells with lower PKCE expression. Furthermore, the siRNA-mediated knockdown or peptide inhibition of PKCE in Ph+ cells increased imatinib-induced apoptosis while overexpression of PKCE reduced imatinib-induced apoptosis, with concomitant increase in the pro-survival factor AKT. Our results suggest PKCE plays a protective role against apoptosis induced by BCR-ABL inhibition in Ph+ leukemias with high PKCE expression, such as Ph+ ALL." @default.
• W1967687440 created "2016-06-24" @default.
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• W1967687440 date "2015-06-19" @default.
• W1967687440 modified "2023-09-23" @default.
• W1967687440 title "Pro-survival role of protein kinase C epsilon in Philadelphia chromosome positive acute leukemia" @default.
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• W1967687440 doi "https://doi.org/10.3109/10428194.2015.1043545" @default.
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