Journal article

The BCL2 selective inhibitor venetoclax induces rapid onset apoptosis of CLL cells in patients via a TP53-independent mechanism

Mary Ann Anderson, Jing Deng, John F Seymour, Constantine Tam, Su Young Kim, Joshua Fein, Lijian Yu, Jennifer R Brown, David Westerman, Eric G Si, Ian J Majewski, David Segal, Sari L Heitner Enschede, David CS Huang, Matthew S Davids, Anthony Letai, Andrew W Roberts

Blood | AMER SOC HEMATOLOGY | Published : 2016

Grants

Awarded by Australian National Health and Medical Research Council


Awarded by Leukemia and Lymphoma Society


Awarded by National Cancer Institute, National Institutes of Health


Funding Acknowledgements

This work was supported by AbbVie, in collaboration with Genentech/Roche. Venetoclax (ABT-199/GDC-0199) is being developed through collaboration between AbbVie and Genentech/Roche. M.A.A. was supported by a fellowship from the Webster bequest. Work in the labs of D.C.S.H. and A.W.R. was supported by scholarships, fellowships, and grants from the Australian National Health and Medical Research Council (research fellowships [A.W.R. and D.C.S.H.], program grants 1016647 and 1016701, and Independent Research Institutes Infrastructure Support Scheme grant 9000220); the Leukemia and Lymphoma Society (SCOR grants 7001-13); the Victorian Cancer Agency; the Cancer Council Victoria; the Australian Cancer Research Foundation; and a Victorian State Government Operational Infrastructure Support grant. This work was supported by a grant from the National Cancer Institute, National Institutes of Health (CA129974) (A.L.). M.S.D. is supported by an American Society of Clinical Oncology Career Development Award.