Bad company: Microenvironmentally mediated resistance to targeted therapy in melanoma

Pigment Cell Melanoma Res. 2019 Mar;32(2):237-247. doi: 10.1111/pcmr.12736. Epub 2018 Oct 18.

Abstract

This review will focus on the role of the tumor microenvironment (TME) in the development of drug resistance in melanoma. Resistance to mitogen-activated protein kinase inhibitors (MAPKi) in melanoma is observed months after treatment, a phenomenon that is often attributed to the incredible plasticity of melanoma cells but may also depend on the TME. The TME is unique in its cellular composition-it contains fibroblasts, immune cells, endothelial cells, adipocytes, and among others. In addition, the TME provides "non-homeostatic" levels of oxygen, nutrients (hypoxia and metabolic stress), and extracellular matrix proteins, creating a pro-tumorigenic niche that drives resistance to MAPKi treatment. In this review, we will focus on how changes in the tumor microenvironment regulate MAPKi resistance.

Keywords: drug resistance; hypoxia; immunology; mechanotransduction; melanoma; oxidative stress.

Publication types

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

MeSH terms

  • Animals
  • Drug Resistance, Neoplasm*
  • Humans
  • Immunity
  • Melanoma / drug therapy*
  • Melanoma / immunology
  • Melanoma / pathology*
  • Mitogen-Activated Protein Kinases / antagonists & inhibitors
  • Mitogen-Activated Protein Kinases / metabolism
  • Molecular Targeted Therapy*
  • Tumor Microenvironment*

Substances

  • Mitogen-Activated Protein Kinases