Melanomagenic gene alterations viewed from a redox perspective: Molecular mechanisms and therapeutic opportunities

Research output: Chapter in Book/Report/Conference proceedingChapter

2 Scopus citations


The causative involvement of altered redox homeostasis and reactive oxygen species (ROS)-dependent signaling in the control of survival, proliferation, and invasiveness of cancer cells has recently emerged. A large body of experimental and epidemiological research has substantiated the causative involvement of specific genetic alterations in melanomagenesis. Strikingly, some of the proteins encoded by specific genes underlying melanomagenesis (CDKN2A, MC1R, MITF, KIT, NRAS, BRAF, AKT3, PTEN, RAC1, MAP3K5, KEAP1, MYC) assume mechanistic roles in the control of cellular redox signaling and oxidative stress, thereby fulfilling molecular functions relevant to suppression or promotion of tumorigenesis that reach beyond their canonical activities, a significant yet underappreciated phenomenon that may open avenues towards novel redox-directed chemotherapeutic interventions as discussed in this chapter.

Original languageEnglish (US)
Title of host publicationStress Response Pathways in Cancer
Subtitle of host publicationFrom Molecular Targets to Novel Therapeutics
PublisherSpringer Netherlands
Number of pages25
ISBN (Electronic)9789401794213
ISBN (Print)9789401794206
StatePublished - Jan 1 2015


  • Chemotherapy
  • Melanocyte
  • Melanoma
  • Melanomagenesis
  • Synthetic lethality
  • Targeted therapeutics

ASJC Scopus subject areas

  • General Medicine
  • General Biochemistry, Genetics and Molecular Biology


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