Login / Signup

CDK4/6-MEK inhibition in MPNSTs causes plasma cell infiltration, sensitization to PD-L1 blockade, and tumor regression.

Jordan L KohlmeyerJoshua J LingoCourtney A KaemmerAmanda SchererAkshaya WarrierEllen VoigtJuan Antonio Raygoza GarayGavin R McGivneyQierra R BrockmanAmy H TangAna CalizoKai PollardXiaochun ZhangAngela C HirbeChristine A PratilasMariah LeidingerPatrick J BrehenyMichael S ChimentiJessica C SierenVarun V MongaMunir R TanasDavid K MeyerholzBenjamin W DarbroRebecca D DoddDawn E Quelle
Published in: Clinical cancer research : an official journal of the American Association for Cancer Research (2023)
CDK4/6-MEK inhibition induces a novel plasma cell-associated immune response and extended antitumor activity in MPNSTs, which dramatically enhances anti-PD-L1 therapy. These preclinical findings provide strong rationale for clinical translation of CDK4/6-MEK-ICB targeted therapies in MPNST as they may yield sustained antitumor responses and improved patient outcomes.
Keyphrases
  • cell therapy
  • cell cycle
  • immune response
  • single cell
  • pi k akt
  • clinical trial
  • stem cells
  • dendritic cells
  • cell proliferation
  • toll like receptor
  • inflammatory response
  • smoking cessation