posted on 2023-04-04, 02:03authored byRobert B. Jones, Jonathan Farhi, Miranda Adams, Kiran K. Parwani, Garrett W. Cooper, Milica Zecevic, Richard S. Lee, Andrew L. Hong, Jennifer M. Spangle
Figure S5 shows that combined PI3K and MLL inhibition provides therapeutic benefit in vitro and in vivo
Funding
HHS | NIH | National Cancer Institute (NCI)
HHS | NIH | National Institute of General Medical Sciences (NIGMS)
U.S. Department of Defense (DOD)
American Cancer Society (ACS)
EU | School of Medicine, Emory University (Emory University School of Medicine)
History
ARTICLE ABSTRACT
Here the authors leverage PI3K/AKT-driven chromatin modification to identify histone methyltransferases as a therapeutic target. Dual PI3K and MLL inhibition synergize to reduce clonogenicity and cell proliferation, and promote in vivo tumor regression. These findings suggest patients with PIK3CA-mutant, HR+ breast cancer may derive clinical benefit from combined PI3K/MLL inhibition.