Journal article
BCL-W is dispensable for the sustained survival of select Burkitt lymphoma and diffuse large B-cell lymphoma cell lines
ST Diepstraten, C Chang, L Tai, JN Gong, P Lan, AC Dowell, GS Taylor, A Strasser, GL Kelly
Blood Advances | Published : 2020
Open access
Abstract
Dysregulated expression of BCL-2 family proteins allows cancer cells to escape apoptosis. To counter this, BH3-mimetic drugs that target and inhibit select BCL-2 prosurvival proteins to induce apoptosis have been developed for cancer therapy. Venetoclax, which targets BCL-2, has been effective as therapy for patients with chronic lymphocytic leukemia, and MCL-1-targeting BH3-mimetic drugs have been extensively evaluated in preclinical studies for a range of blood cancers. Recently, BCL-W, a relatively understudied prosurvival member of the BCL-2 protein family, has been reported to be abnormally upregulated in Burkitt lymphoma (BL), diffuse large B-cell lymphoma (DLBCL), and Hodgkin lymphoma..
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Awarded by Victorian Cancer Agency
Funding Acknowledgements
This work was supported by funding from the Victorian Cancer Agency Fellowship (MCRF 17028) (G.L.K.), Cancer Council Victoria, grants-in-aid #1086157 and #1147328 (G.L.K.), the National Health and Medical Research Council (grant 1086291) (G.L.K.), Program grant 101671 (A.S.), Fellowship 1020363 (A.S.), Leukaemia Foundation Australia grant (G.L.K. and A.S.), Leukaemia and Lymphoma Society (grant 7001-13) (A.S.), the estate of Anthony (Toni) Redstone OAM, The Craig Perkins Cancer Research Foundation, and operational infrastructure grants through the Australian Government National Health and Medical Research Council Independent Research Institutes Infrastructure Support Scheme and the Victorian State Government Operational Infrastructure Support.