Making the discoveries that defeat cancer

  • Home |
  • About Us  |
  • Research  |
  • Enterprise  |
  • Education  |
  • Jobs  |
  • Support Us  |
  • News  |
  • Contact Us
  • Home »
  • Research »
  • Research Highlights »
  • Research Highlight Archive

Research

  • ICR Ranking on RAE
  • Research Highlights
  • Publications Repository
  • Research Divisions
  • Team Leaders
  • Biomedical Research Centre
  • REF 2014

Genetic Mutation Shown to Trigger Melanoma

1 June 2010 - ICR researchers have discovered that a genetic mutation found in some malignant melanomas can initiate development of this most deadly form of skin cancer. 

The family of RAS genes normally control cell growth during development and other processes such as wound healing, but they can stimulate cancer development when they malfunction.  One of these genes, KRAS, was already known to be mutated in about two per cent of malignant melanomas, but Professor Richard Marais and colleagues at the ICR are the first to show that damage to this gene can be the first in a procession of genetic events necessary to trigger malignant melanoma.

The team created an animal model that mimicked how humans acquire mutations in KRAS. Although KRAS mutations were identified as the possible first event in melanoma development, other genetic mutations are thought to be necessary to promote cancer growth. The disease is difficult to treat once it has spread to other organs and it is hoped that the identification of these other changes will allow new therapeutic approaches to be developed.

 “We know that the main cause of skin cancer is damage driven by the UV rays in sunlight, and we are now building up a picture of the key genes involved in this disease,” Professor Marais said.

Back to other research highlights

Related Links


Last updated: 11 June 2010

The Royal Marsden - NHS foundation trust
  • Contacts  | 
  • Privacy  | 
  • Terms and Conditions  | 
  • Accessibility  | 
  • Feedback  | 
  • Cookies  | 
  • Status
  • ICR News RSS Feed
  • Find us on Facebook
  • Follow us on Twitter