Melanoma is a deadly and the most aggressive skin cancer, and long-term exposure to GSTM2 sunlight under the relevant. Recently, researchers from the Dana-Farber Cancer Institute and Broad Institute, a whole-genome sequencing of 25 metastatic melanoma, the researchers confirmed that chronic sunlight exposure in the development of melanoma inrole, and reveals the important genetic changes in melanoma. The research results were published in the international journal Nature on May 19.In the GSTM4 article, the researchers demonstrated in human melanoma high-resolution genome landscape, previous genetic analysis of the focus on the many types of melanoma exon group, and researchers concerned about is some small fragments of genetic code to produce the protein genes. The researchers said that the melanoma genome contains a wealth of genetic information, sequencing of 25 metastatic melanoma, the scientists GSTO1 melanoma changes in genetic diversity.Melanoma, whole-genome sequencing will be found in some abundance, and these exon groups can not be captured discovered researchers Levi A.Garraway said. Through whole-genome sequencing, you will see more precisely the proportion of melanoma gene mutations and different types of GSTP1 mutations, so we have more confidence to describe melanoma caused by UV induced gene mutation or mutagenesis. When scientists develop a melanoma genome data and their extensive analysis, they found that the patient's genetic mutation and chronic sunlight exposure, it is even more determined the influence of sunlight damage for the development of melanoma.
Analysis of the entire genome of the GSTT1 human melanoma, the first show the existence of the structural rearrangement of the many types of tumors, as expected, scientists have known BRAF mutations and NRAS mutations detected in 24 types of tumors, these genes the transfer of important signaling molecules involved in cell growth. More interestingly the gene PREX2, the gene can be shut down tumor known genes to make the patients suffering from breast cancer and mutations in 44% of patients; PREX2 genetic broken gathered mutation, and can accelerate tumor development, mutations not only occur in the designated location, but can be a classic open oncogene. Researchers Berger said, this style of mutations and tumor suppressor genes very much like, but from the functional experiments, it acts more like a cancer gene.When PREX2 function properly, it will react with the protein PTEN, PTEN is a tumor suppressor gene, can stand for the growth of normal cells and mice show that, mutation of PREX2 can stimulate tumor growth. The researchers said that now they still unclear how to work for PREX2 PREX2 may be classified as a new cancer gene types, the researchers the future will depend on the gene for a new a new target for the treatment of melanoma.Perhaps PREX2 discovery is only the tip of the iceberg, as if the discovery of PREX2 new melanoma genes remain to be discovered through new technologies.