Journal article

BH3 Mimetics for the Treatment of B-Cell Malignancies-Insights and Lessons from the Clinic

Victor S Lin, Zhuo-Fan Xu, David CS Huang, Rachel Thijssen

CANCERS | MDPI | Published : 2020

Abstract

The discovery of the link between defective apoptotic regulation and cancer cell survival engendered the idea of targeting aberrant components of the apoptotic machinery for cancer therapy. The intrinsic pathway of apoptosis is tightly controlled by interactions amongst members of three distinct subgroups of the B-cell lymphoma 2 (BCL2) family of proteins. The pro-survival BCL2 proteins prevent apoptosis by keeping the pro-apoptotic effector proteins BCL2-associated X protein (BAX) and BCL2 homologous antagonist/killer (BAK) in check, while the BH3-only proteins initiate apoptosis by either neutralizing the pro-survival BCL2 proteins or directly activating the pro-apoptotic effector proteins..

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University of Melbourne Researchers

Grants

Awarded by Australian National Health and Medical Research Council (NHMRC)


Awarded by Specialized Center of Research [SCOR] grant from the Leukemia and Lymphoma Society


Awarded by Leukemia and Lymphoma Society


Funding Acknowledgements

Z.-F.X. is supported by a Scholarship from China Scholarship Council. D.C.S.H. is supported by Fellowship (1156024) and a Program Grant (1016701) from the Australian National Health and Medical Research Council (NHMRC) and a Specialized Center of Research [SCOR] grant (7015-18) from the Leukemia and Lymphoma Society. R.T. is supported by a Fellowship (5467-18) from the Leukemia and Lymphoma Society.