Metabolic modulation by CDK4/6 inhibitor promotes chemokine-mediated recruitment of T cells into mammary tumors
Roman V. Uzhachenko, Vijaya Bharti, Zhufeng Ouyang, Ashlyn Blevins, Stacey Mont, Nabil Saleh, Hunter Lawrence, Chengli Shen, Sheau‐Chiann Chen, Gregory D. Ayers, David G. DeNardo, Carlos L. Arteaga, Ann Richmond, Anna E. Vilgelm
Abstract
(Cell Reports 35, 108944-1–16.e1–e6; April 6, 2021) Carlos Arteaga receives or has received research grants from Pfizer, Lilly, and Takeda; holds minor stock options in Provista; serves or has served in an advisory role to Novartis, Merck, Lilly, Daiichi Sankyo, Taiho Oncology, OrigiMed, Puma Biotechnology, Immunomedics, AstraZeneca, Arvinas, and Sanofi; and reports scientific advisory board remuneration from the Susan G. Komen Foundation. None of these relationships are relevant to the work published in this manuscript. This information was inadvertently omitted during the preparation of the manuscript but now appears with the article online. The authors regret this error. Metabolic modulation by CDK4/6 inhibitor promotes chemokine-mediated recruitment of T cells into mammary tumorsUzhachenko et al.Cell ReportsApril 06, 2021In BriefInhibitors of cell cycle kinases CDK4/6 delay progression of metastatic breast cancer; however, they do not eliminate tumors. Uzhachenko et al. report that metabolic changes in CDK4/6 inhibitor-treated cancer cells make them vulnerable to T cell therapies. These data highlight potential utility of CDK4/6 inhibitors to overcome immunotherapy resistance. Full-Text PDF Open Access