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CDK4 selective inhibition improves preclinical anti-tumor efficacy and safety

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By Cynthia Palmer, Britton Boras, Scott Garza, Jing Yuan, Tae Sung, Elizabeth McMillan Verified, Na Wei, James Oakley, Lisa Nguyen, Ping Chen, Eric Johnson, Xiu Yu, Wade C. Diehl, Gary M. Gallego, Rose Ann Ferre, Sujin Cho-Schultz, Hong Shen, Qin Zhang, Timothy R. Baffi, Meirong Xu, Whijae Roh, Jérôme Goudeau, Yanke Yu, Rajat Gupta, Kimberly Kim, Stephen Dann, Zhengyan Kan, Nichol Miller, Andrew R. Nager, Casey Quinlan Verified, Cathy Zhang, Todd L. VanArsdale, Bernadette Pascual, Danan Li, Nanni Huser, Julie A. Cianfrogna, Jason Carmody, Aubrey Nayeon Kang, Seth Darensburg, Taran Dodd, James Solowiej, Suvi T.M. Orr, Mehran Jalaie, Judith G. Deal, Jennifer Lapira-Miller, John C. Kath, Sajiv K. Nair, Brion W. Murray, Matthew D. Petroski, Aida Sacaan, Lars Anders
| Cell Press Verified
Keywords atirmociclib PF-07220060 CDK4 cyclin D1 breast cancer cell cycle cell cycle inhibitor neutropenia cyclin-dependent kinase CDK6 Introduction Aberrant cell proliferation is a fundamental hallmark of human cancer.1 In tumor cells, it is frequently orchestrated by cyclin D-dependent kinases, CDK4 and CDK6; each kinase forms active complexes with one of the three D-type cyclins (D1, D2, or D3).
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