The CDK4/6 Inhibitor Abemaciclib Induces a T Cell Inflamed Tumor Microenvironment and Enhances the Efficacy of PD-L1 Checkpoint Blockade

Cell Rep. 2018 Mar 13;22(11):2978-2994. doi: 10.1016/j.celrep.2018.02.053.

Abstract

Abemaciclib, an inhibitor of cyclin dependent kinases 4 and 6 (CDK4/6), has recently been approved for the treatment of hormone receptor-positive breast cancer. In this study, we use murine syngeneic tumor models and in vitro assays to investigate the impact of abemaciclib on T cells, the tumor immune microenvironment and the ability to combine with anti-PD-L1 blockade. Abemaciclib monotherapy resulted in tumor growth delay that was associated with an increased T cell inflammatory signature in tumors. Combination with anti-PD-L1 therapy led to complete tumor regressions and immunological memory, accompanied by enhanced antigen presentation, a T cell inflamed phenotype, and enhanced cell cycle control. In vitro, treatment with abemaciclib resulted in increased activation of human T cells and upregulated expression of antigen presentation genes in MCF-7 breast cancer cells. These data collectively support the clinical investigation of the combination of abemaciclib with agents such as anti-PD-L1 that modulate T cell anti-tumor immunity.

Keywords: CDK4/6; PD-1; PD-L1; abemaciclib; cancer; combination immunotherapy.

MeSH terms

  • Aminopyridines / pharmacology
  • Aminopyridines / therapeutic use*
  • Benzimidazoles / pharmacology
  • Benzimidazoles / therapeutic use*
  • Cyclin-Dependent Kinase Inhibitor p15 / pharmacology
  • Cyclin-Dependent Kinase Inhibitor p15 / therapeutic use*
  • Cyclin-Dependent Kinase Inhibitor p18 / pharmacology
  • Cyclin-Dependent Kinase Inhibitor p18 / therapeutic use*
  • Humans
  • Programmed Cell Death 1 Receptor / metabolism*
  • Tumor Microenvironment

Substances

  • Aminopyridines
  • Benzimidazoles
  • Cyclin-Dependent Kinase Inhibitor p15
  • Cyclin-Dependent Kinase Inhibitor p18
  • Programmed Cell Death 1 Receptor
  • abemaciclib