Bad company: Microenvironmentally mediated resistance to targeted therapy in melanoma

Filipe V. Almeida, Stephen M. Douglass, Mitchell E. Fane, Ashani T. Weeraratna

Research output: Contribution to journalReview articlepeer-review

16 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)237-247
Number of pages11
JournalPigment Cell and Melanoma Research
Issue number2
StatePublished - Mar 1 2019
Externally publishedYes


  • drug resistance
  • hypoxia
  • immunology
  • mechanotransduction
  • melanoma
  • oxidative stress

ASJC Scopus subject areas

  • Oncology
  • Biochemistry, Genetics and Molecular Biology(all)
  • Dermatology


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