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Target Oncol. 2018 Feb;13(1):21-38. doi: 10.1007/s11523-017-0541-2.

Inhibiting CDK in Cancer Therapy: Current Evidence and Future Directions.

Author information

1
Department of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, 6565 MD Anderson Blvd; Z6.2030, Houston, TX, 77030, USA.
2
Department of Breast Medical Oncology, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd., Unit 1354; CPB5.3542, Houston, TX, 77030, USA.
3
Department of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, 6565 MD Anderson Blvd., Unit 0066; Z6.3012, Houston, TX, 77030, USA.
4
Department of Breast Medical Oncology, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Unit 1354, Houston, TX, 77030-4009, USA. rlayman@mdanderson.org.

Abstract

Cell cycle dysregulation is a hallmark of all cancers, resulting in uncontrolled proliferation. Cyclin dependent kinases (CDKs), a family of proteins that are involved in the regulation of the cell cycle, are frequently overexpressed or mutated in cancer. Hence, CDK-inhibiting drugs have been developed and evaluated as cancer therapeutics. Clinical trials have shown CDK4/6 inhibitors (CDK4/6i) to be relatively safe and effective, and these are now standard of care treatment for advanced hormone receptor positive breast cancer. Some CDK4/6i drugs are also able to cross the blood brain barrier and may, therefore, offer effective therapy for primary and metastatic central nervous system malignancies. Ongoing research is also evaluating CDK4/6i for additional breast cancer subtypes and non-breast malignancies with promising early phase clinical trial results. Finally, pre-clinical research has identified potential biomarkers for CDK4/6i efficacy and is exploring potential resistance mechanisms to this treatment. Further clinical-translational research is needed to advance patient selection and combinatorial treatment strategies with CDK4/6i in breast cancer and other malignancies.

PMID:
29218622
DOI:
10.1007/s11523-017-0541-2
[Indexed for MEDLINE]

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