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
<p>Figure S5 shows that combined PI3K and MLL inhibition provides therapeutic benefit in vitro and in vivo</p>
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)
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.