CONCLUSION
The benefits of CDK4/6i’s in PCa can be optimized by fully understanding pathways that are involved with the cell cycle, resistance patterns of CDK4/6i’s and by utilizing therapies that target driver mutations in mCRPC. Additional research is needed in these key areas in order to provide more insightful reasoning to combinatorial therapies with CDK4/6i’s to maximize efficacy and durability of response. The best opportunity for synergistic success occurs when agents are combined based on interrelated mechanisms, resistance profiles, and genomics, however, it is extremely important to consider the adverse effects of the combined agents. Precision medicine should not only aid with improving effectiveness of treatment, but also protect and identify patients who would not benefit from therapy thus avoiding toxicity and decreasing morbidity. Novel strategic combinatorial therapies for mCRPC, with a CDK4/6i as the common backbone, have the potential to improve overall survival and quality of life in a patient population with few therapeutic options.
Acknowledgments
Julie Nielsen, Mayo Clinic senior production designer.
Disclosure
The authors report no conflicts of interest in this work.
Adam M Kase,1 John A Copland III,2 Winston Tan1
1Mayo Clinic Florida Division of Hematology Oncology, Jacksonville, FL 32224, USA; 2Mayo Clinic Florida Department of Cancer Biology, Jacksonville, FL 32224, USA
Correspondence: Adam M Kase Tel +1 904-953-0315
Fax +1 905-953-2315
Email [email protected]
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Source: OncoTargets and Therapy.
Originally published October 15, 2020.
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