Genomic Aberrations that Activate D-type Cyclins Are Associated with Enhanced Sensitivity to the CDK4 and CDK6 Inhibitor Abemaciclib

Cancer Cell. 2017 Dec 11;32(6):761-776.e6. doi: 10.1016/j.ccell.2017.11.006.

Abstract

Most cancers preserve functional retinoblastoma (Rb) and may, therefore, respond to inhibition of D-cyclin-dependent Rb kinases, CDK4 and CDK6. To date, CDK4/6 inhibitors have shown promising clinical activity in breast cancer and lymphomas, but it is not clear which additional Rb-positive cancers might benefit from these agents. No systematic survey to compare relative sensitivities across tumor types and define molecular determinants of response has been described. We report a subset of cancers highly sensitive to CDK4/6 inhibition and characterized by various genomic aberrations known to elevate D-cyclin levels and describe a recurrent CCND1 3'UTR mutation associated with increased expression in endometrial cancer. The results suggest multiple additional classes of cancer that may benefit from CDK4/6-inhibiting drugs such as abemaciclib.

Keywords: CCND1; CCND2; CCND3; CDK2; CDKN2A.

MeSH terms

  • Aminopyridines / pharmacology*
  • Animals
  • Antineoplastic Agents / pharmacology
  • Benzimidazoles / pharmacology*
  • Cell Proliferation / drug effects
  • Clinical Trials, Phase I as Topic
  • Cyclin D / genetics
  • Cyclin D / metabolism*
  • Cyclin-Dependent Kinase 4 / antagonists & inhibitors
  • Cyclin-Dependent Kinase 6 / antagonists & inhibitors
  • Female
  • Humans
  • Mice
  • Mice, Inbred BALB C
  • Mice, Nude
  • Neoplasms / drug therapy
  • Neoplasms / genetics*
  • Neoplasms / metabolism
  • Xenograft Model Antitumor Assays

Substances

  • Aminopyridines
  • Antineoplastic Agents
  • Benzimidazoles
  • Cyclin D
  • abemaciclib
  • Cyclin-Dependent Kinase 4
  • Cyclin-Dependent Kinase 6