<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Margetis, Nikolaos</style></author><author><style face="normal" font="default" size="100%">Kouloukoussa, Myrsini</style></author><author><style face="normal" font="default" size="100%">Pavlou, Kyriaki</style></author><author><style face="normal" font="default" size="100%">Vrakas, Spyridon</style></author><author><style face="normal" font="default" size="100%">Mariolis-Sapsakos, Theodoros</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">K- Mutations as the Earliest Driving Force in a Subset of Colorectal Carcinomas.</style></title><secondary-title><style face="normal" font="default" size="100%">In Vivo</style></secondary-title><alt-title><style face="normal" font="default" size="100%">In Vivo</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adenomatous Polyposis Coli Protein</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Transformation, Neoplastic</style></keyword><keyword><style  face="normal" font="default" size="100%">Colon</style></keyword><keyword><style  face="normal" font="default" size="100%">Colorectal Neoplasms</style></keyword><keyword><style  face="normal" font="default" size="100%">DNA Breaks, Double-Stranded</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Mutation</style></keyword><keyword><style  face="normal" font="default" size="100%">Proto-Oncogene Proteins p21(ras)</style></keyword><keyword><style  face="normal" font="default" size="100%">Reactive Oxygen Species</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2017</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2017 Jul-Aug</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">31</style></volume><pages><style face="normal" font="default" size="100%">527-542</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">K-ras oncogene is a key factor in colorectal cancer. Based on published and our data we propose that K-ras could be the oncogene responsible for the inactivation of the tumor-suppressor gene APC, currently considered as the initial step in colorectal tumorigenesis. K-ras fulfills the criteria of the oncogene-induced DNA damage model, as it can provoke well-established causes for inactivating tumor-suppressors, i.e. DNA double-strand breaks (causing allele deletion) and ROS production (responsible for point mutation). The model we propose is a variation of the currently existing model and hypothesizes that, in a subgroup of colorectal carcinomas, K-ras mutation may precede APC inactivation, representing the earliest driving force and, probably, an early biomarker of colorectal carcinogenesis. This observation is clinically useful, since it may modify the preventive colorectal cancer strategy, restricting numerically patients undergoing colonoscopies to those bearing K-ras mutation in their colorectum, either in benign polyps or the normal accompanying mucosa.</style></abstract><issue><style face="normal" font="default" size="100%">4</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/28652417?dopt=Abstract</style></custom1></record></records></xml>