Scratching the Surface: NECTIN-4 as a Surrogate for Enfortumab Vedotin Resistance

Clin Cancer Res. 2023 Apr 14;29(8):1377-1380. doi: 10.1158/1078-0432.CCR-22-3882.

Abstract

Clinical data with enfortumab vedotin (EV) suggest that most bladder cancers overexpress NECTIN-4. A recent article shows that NECTIN-4 membranous expression changes with progression to metastatic disease and that low NECTIN-4 expression in metastatic biopsies is potentially associated with EV resistance. These data argue for incorporation of NECTIN-4 expression into future biomarker strategies. See related article by Klümper et al., p. 1496.

Publication types

  • Editorial
  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Comment

MeSH terms

  • Antibodies, Monoclonal / pharmacology
  • Antibodies, Monoclonal / therapeutic use
  • Carcinoma, Transitional Cell*
  • Cell Adhesion Molecules / genetics
  • Cell Adhesion Molecules / metabolism
  • Humans
  • Nectins
  • Urinary Bladder Neoplasms* / drug therapy
  • Urinary Bladder Neoplasms* / genetics
  • Urinary Bladder Neoplasms* / pathology

Substances

  • enfortumab vedotin
  • Nectins
  • Antibodies, Monoclonal
  • Cell Adhesion Molecules