Researchers of the Melanoma group at the Vall d'Hebron Institute of Research (VHIR), integrated by professionals from the services of Dermatology, Oncology and Pathology, and led by Dr. Juan ángel Recio, discovered that a protein, called LKB1, is essential to trigger the process of reparation of the DNA damage caused by solar radiation. The landmark, published in "http://www.plosgenetics.org/article/info%3Adoi/10.1371/journal.pgen.1004721?utm_source=feedburner&utm_medium=feed&utm_campaign=Feed%3A+plosgenetics/NewArticles+%28PLOS+Genetics+-+New+Articles%29" Plos Genetics, paves the way for the use of the protein as a prognostic factor in patients with ultraviolet induced skin cancer. Ultraviolet radiation has been associated to the acquisition of different types of skin cancer and premature skin aging. It causes modifications in the genetic material of cells (DNA) that if not repaired properly will lead to a mutated DNA which might trigger the development of cancer. In fact, several studies conclude that people who overexposed to the sun during their childhood are more likely to develop melanoma at the age of 50 and above. For that reason, understanding the molecular basis of the ultraviolet-induced DNA damage response is important to elucidate the mechanisms of skin tumorigenesis.The aim of the study was to determine the causes that lead to the development of skin cancer due to ultraviolet radiation. Particularly, they wanted to unveil how LKB1, which is a mutant protein in humans, participates in these processes. Firstly, the authors used a UV-induced skin cancer mouse model, where one of the two Lkb1 gene alleles was deleted, and consequently the amounts of LKB1 protein was of half the normal levels. A single dose of ultraviolet radiation in Lkb1 neonate mice was enough to induce the quick development of squamous cell carcinomas, and this was associated to a deficient response in DNA damage repair. This single dose of radiation is the equivalent to three hours of exposure to the sun without any protection in summer. The results were surprising, Dr. Recio reported, because the animals developed skin cancer five months before the expected date: "mice with the protein inactivated in one allel developed, in just one month, a type of cancer that use to suffer farmers, fishermen or people who has been exposed to the sun for a long period in their life", explained Dr. Recio. Moreover, cells harboring the damaged DNA were resistant to cell death (apoptosis). Thus, as Dr. Recio said, lack of LKB1 promotes a double effect: "cells not only fail to repair the damage in their DNA, but they do not die, leading to the accumulation of mutated cells and the development of tumors". The research team has obtained similar results (to be published soon) in two additional mouse models of melanoma, a much more lethal type of UV-induced skin cancer. In the near future, Dr. Recio's team will be evaluating LKB1 as a prognostic risk factor for ultraviolet-induced skin cancer. They also are investigating the different factors that may alter LKB1 expression, with a particular emphasis in families with skin cancer predisposition or skin cancer history.