Harnessing the PD-1 pathway in renal cell carcinoma: current evidence and future directions

BioDrugs. 2014 Dec;28(6):513-26. doi: 10.1007/s40259-014-0111-4.

Abstract

Programmed cell death-1 (PD-1) is a recognized immune checkpoint. It is frequently upregulated on the T cells that infiltrate tumors, providing an inhibitory signal, which may facilitate immune escape. Blocking antibodies have been developed to interrupt the interaction of PD-1 with its ligands PD-L1/PD-L2, with the goal of increasing the host antitumor immune response. Initial results have been encouraging, with durable responses in both treatment-naive and pretreated patients, along with an acceptable toxicity profile. This tolerability makes PD-1 blockade an excellent potential partner for combination strategies with the approved targeted agents, such as tyrosine kinase inhibitors (TKIs) and anti-vascular endothelial growth factor (anti-VEGF) antibodies, as well as other investigational immune checkpoint inhibitors or agonist antibodies that may costimulate an immune response. PD-L1 expression on tumor cells and tumor-infiltrating immune cells is also being evaluated as a predictive biomarker of response to treatment. This review summarizes the biological basis, preclinical studies, ongoing trials, and future challenges associated with targeting the PD-1 pathway in renal cell carcinoma.

Publication types

  • Review

MeSH terms

  • Animals
  • Antibodies / immunology
  • Antibodies / pharmacology*
  • Antibodies / therapeutic use*
  • Antineoplastic Agents / immunology
  • Antineoplastic Agents / pharmacology*
  • Antineoplastic Agents / therapeutic use*
  • Carcinoma, Renal Cell / drug therapy*
  • Carcinoma, Renal Cell / immunology
  • Carcinoma, Renal Cell / metabolism*
  • Clinical Trials as Topic
  • Drug Evaluation, Preclinical
  • Humans
  • Programmed Cell Death 1 Receptor / immunology
  • Programmed Cell Death 1 Receptor / metabolism*
  • Randomized Controlled Trials as Topic
  • Signal Transduction / drug effects
  • Signal Transduction / immunology

Substances

  • Antibodies
  • Antineoplastic Agents
  • Programmed Cell Death 1 Receptor