30 March 2009

Skin Cancer Study Uncovers New Tumor Suppressor Gene

A recent study on skin cancer has been able to identify a specific gene which has the ability to suppress tumor growth melanoma cases. Melanoma is regarded as the deadliest form of skin cancer, responsible for the majority of skin cancer related deaths, estimated to be around 48,000 each year. Researchers from the National Institute of Health (NIH) lead are leading the investigation and have studied a collection of tumor and blood samples collected from 79 petients with aggressive melanoma. Through the analysis of this study te researchers found that a quarter of melanoma tumors involved mutations in the genes that cod for matrix metalloproteinase (MMP) enzymes. The researchers believe the findings of this study will lead to more specialized cancer treatment options in which MMP enzymes are involved.
A tumor suppressor gene encodes proteins which slow or even stop cell growth, and oncogenes are genes which encode proteins involved in normal cell growth. If either of these types’ genes is mutated they are unable to function correctly resulting in the growth of cancer. Therefore cancer therapies targeted at oncogenes aim to reduce their action, while therapies targeted at suppressor genes aim to increase their action. The genes which code MMP enzymes have always been thought to be oncogenes however this study shows the most common mutations of MMP genes in melanoma are not at all oncogenes. The researchers found that MMP-8, a common mutated form, actually acts as a suppressor gene. This finding is able to explain why cancer drugs aimed to block MMP enzymes have a very poor performance record. Therefore this study has the potential to dramatically change the way in which cancer is treated, the findings suggest the best approach is to develop drugs which inhibit only the MMP’s which are oncogenes or drugs which enhance MMP-8.

Article Reference:
'Skin Cancer Study Uncovers New Tumor Suppressor Gene' 2009, Nature Genetics , March 2009, viewed 30 March 2009, .