Journal article
BCL-W makes only minor contributions to MYC-driven lymphoma development
ST Diepstraten, JE La Marca, C Chang, S Young, A Strasser, GL Kelly
Oncogene | SPRINGERNATURE | Published : 2023
Abstract
The BH3-mimetic drug Venetoclax, a specific inhibitor of anti-apoptotic BCL-2, has had clinical success for the treatment of chronic lymphocytic leukaemia and acute myeloid leukaemia. Attention has now shifted towards related pro-survival BCL-2 family members, hypothesising that new BH3-mimetic drugs targeting these proteins may emulate the success of Venetoclax. BH3-mimetics targeting pro-survival MCL-1 or BCL-XL have entered clinical trials, but managing on-target toxicities is challenging. While increasing evidence suggests BFL-1/A1 is a resistance factor for diverse chemotherapeutic agents and BH3-mimetic drugs in haematological malignancies, few studies have explored the role of BCL-W i..
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Funding Acknowledgements
This work was supported by fellowships and grants from the Australian National Health and Medical Research Council (NHMRC) (Program Grant GNT1113133 to AS, Research Fellowship GNT1116937 to AS, Project Grant GNT1143105 to AS, Ideas Grants GNT 2002618 and GNT2001201 to GLK, Synergy Grants GNT2011139 to GLK and GNT2010275 to AS), the Leukemia & Lymphoma Society of America (Specialised Center of Research [SCOR] grant no. 7015-18 to AS and GLK), Victorian Cancer Agency (MCRF Fellowship 17028 to GLK and ECRF Fellowship 21006 to STD), CASS Foundation Grants (to STD and JELM), the estate of Anthony (Toni) Redstone OAM (AS and GLK), the Craig Perkins Cancer Research Foundation (GLK), the Dyson Bequest (GLK) and the Harry Secomb Foundation (GLK), and operational infrastructure grants through the Victorian State Government Operational Infrastructure Support (OIS) and Australian Government NHMRC Independent Research Institute Infrastructure Support (IRIIS) Schemes. Open Access & nbsp;funding & nbsp;enabled and organized by CAUL and its Member Institutions.