Abstract
Abstract CDK4/6 inhibitors (CDK4/6i) in combination with antiestrogens have revolutionized the treatment of ER+ metastatic breast cancer (MBC), significantly prolonging survival. However, this combination is not curative in MBC, and resistance to CDK4/6i represents a major challenge. A diverse array of mechanisms of CDK4/6i resistance have been described, including deregulation of the G1/S cell cycle checkpoint (i.e. Rb, Cyclin E/CDK2, CDK6, INK4s), activation of growth factor signaling pathways (receptor tyrosine kinases, Ras/MAPK pathway, PI3K/AKT pathway), and contributions from the tumor microenvironment. A detailed understanding of these mechanisms is critical for overcoming CDK4/6i resistance. In this presentation, I will discuss recent advances in defining novel biomarkers that are causally associated with CDK4/6i resistance, therapeutic vulnerabilities linked to distinct mechanisms of resistance, and potential strategies to improve clinical responses to CDK4/6i in ER+ MBC. Citation Format: Ariella Hanker. CDK4/6 inhibitor resistance: Biological mechanisms and novel approaches [abstract]. In: Proceedings of the 2022 San Antonio Breast Cancer Symposium; 2022 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2023;83(5 Suppl):Abstract nr F4-1.
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