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Current Therapeutic Progress of CDK4/6 Inhibitors in Breast Cancer

Yanmei Wu1, Yu Zhang2, Hao Pi1

  • 1Department of Breast and Thyroid Surgery, Changhai Hospital, Navy Medical University, Shanghai 200433, People's Republic of China.

Cancer Management and Research
|June 12, 2020
PubMed

Insights

Cyclin-dependent kinase (CDK) 4/6 inhibitors significantly improve outcomes for advanced hormone receptor-positive breast cancer when combined with endocrine therapy. This review covers their clinical use, trials, survival data, biomarkers, and resistance mechanisms.

Area of Science:

  • Oncology
  • Pharmacology

Background:

  • Selective cyclin-dependent kinase (CDK) 4/6 inhibitors have transformed treatment for hormone receptor (HR)-positive, human epidermal growth factor receptor 2 (HER2)-negative advanced or metastatic breast cancer (ABC/mBC).
  • These inhibitors, combined with endocrine therapy (ET), demonstrate substantial improvements in progression-free survival (PFS) compared to ET alone.

Purpose of the Study:

  • To review the current clinical applications of CDK4/6 inhibitors in HR+/HER2- ABC/mBC.
  • To summarize ongoing clinical trials, overall survival data, and explore potential biomarkers and resistance mechanisms associated with CDK4/6 inhibitors.

Main Methods:

  • Literature review of clinical trials and published data on CDK4/6 inhibitors.
  • Analysis of efficacy, safety, biomarker studies, and resistance patterns.

Main Results:

  • Three CDK4/6 inhibitors (palbociclib, ribociclib, abemaciclib) are FDA and EMA approved for HR+/HER2- ABC/mBC.
  • Combination therapy with ET significantly enhances PFS and, in some cases, overall survival.
  • Research is ongoing to identify predictive biomarkers and overcome resistance.

Conclusions:

  • CDK4/6 inhibitors are a cornerstone therapy for HR+/HER2- ABC/mBC, offering improved PFS and survival.
  • Understanding biomarkers and resistance mechanisms is crucial for optimizing treatment strategies and future drug development.
Keywords:
CDK4/6 inhibitorbreast cancerclinical efficacymechanismresistance

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