<?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%">Alvarez, S.</style></author><author><style face="normal" font="default" size="100%">Diaz-Uriarte, R.</style></author><author><style face="normal" font="default" size="100%">Osorio, A.</style></author><author><style face="normal" font="default" size="100%">Barroso, A.</style></author><author><style face="normal" font="default" size="100%">Melchor, L.</style></author><author><style face="normal" font="default" size="100%">Paz, M. F.</style></author><author><style face="normal" font="default" size="100%">Honrado, E.</style></author><author><style face="normal" font="default" size="100%">Rodriguez, R.</style></author><author><style face="normal" font="default" size="100%">Urioste, M.</style></author><author><style face="normal" font="default" size="100%">Valle, L.</style></author><author><style face="normal" font="default" size="100%">Diez, O.</style></author><author><style face="normal" font="default" size="100%">Cigudosa, J. C.</style></author><author><style face="normal" font="default" size="100%">Dopazo, J.</style></author><author><style face="normal" font="default" size="100%">Esteller, M.</style></author><author><style face="normal" font="default" size="100%">Benitez, J.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">A predictor based on the somatic genomic changes of the BRCA1/BRCA2 breast cancer tumors identifies the non-BRCA1/BRCA2 tumors with BRCA1 promoter hypermethylation</style></title><secondary-title><style face="normal" font="default" size="100%">Clin Cancer Res</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">BRCA1 Protein/*genetics BRCA2 Protein/*genetics Breast Neoplasms/*genetics/pathology Chromosomes</style></keyword><keyword><style  face="normal" font="default" size="100%">Genetic/*genetics</style></keyword><keyword><style  face="normal" font="default" size="100%">Human</style></keyword><keyword><style  face="normal" font="default" size="100%">Human Humans Male Mutation Nucleic Acid Hybridization/methods Promoter Regions</style></keyword><keyword><style  face="normal" font="default" size="100%">Pair 12/genetics Chromosomes</style></keyword><keyword><style  face="normal" font="default" size="100%">Pair 15/genetics Chromosomes</style></keyword><keyword><style  face="normal" font="default" size="100%">Pair 18/genetics Chromosomes</style></keyword><keyword><style  face="normal" font="default" size="100%">Pair 2/genetics Chromosomes</style></keyword><keyword><style  face="normal" font="default" size="100%">Pair 8/genetics *DNA Methylation Female Genome</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2005</style></year></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=15709182</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">3</style></number><volume><style face="normal" font="default" size="100%">11</style></volume><pages><style face="normal" font="default" size="100%">1146-53</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">The genetic changes underlying in the development and progression of familial breast cancer are poorly understood. To identify a somatic genetic signature of tumor progression for each familial group, BRCA1, BRCA2, and non-BRCA1/BRCA2 (BRCAX) tumors, by high-resolution comparative genomic hybridization, we have analyzed 77 tumors previously characterized for BRCA1 and BRCA2 germ line mutations. Based on a combination of the somatic genetic changes observed at the six most different chromosomal regions and the status of the estrogen receptor, we developed using random forests a molecular classifier, which assigns to a given tumor a probability to belong either to the BRCA1 or to the BRCA2 class. Because 76.5% (26 of 34) of the BRCAX cases were classified with our predictor to the BRCA1 class with a probability of &gt;50%, we analyzed the BRCA1 promoter region for aberrant methylation in all the BRCAX cases. We found that 15 of the 34 BRCAX analyzed tumors had hypermethylation of the BRCA1 gene. When we considered the predictor, we observed that all the cases with this epigenetic event were assigned to the BRCA1 class with a probability of &gt;50%. Interestingly, 84.6% of the cases (11 of 13) assigned to the BRCA1 class with a probability &gt;80% had an aberrant methylation of the BRCA1 promoter. This fact suggests that somatic BRCA1 inactivation could modify the profile of tumor progression in most of the BRCAX cases.</style></abstract><notes><style face="normal" font="default" size="100%">Alvarez, Sara Diaz-Uriarte, Ramon Osorio, Ana Barroso, Alicia Melchor, Lorenzo Paz, Maria Fe Honrado, Emiliano Rodriguez, Raquel Urioste, Miguel Valle, Laura Diez, Orland Cigudosa, Juan Cruz Dopazo, Joaquin Esteller, Manel Benitez, Javier Comparative Study Research Support, Non-U.S. Gov’t United States Clinical cancer research : an official journal of the American Association for Cancer Research Clin Cancer Res. 2005 Feb 1;11(3):1146-53.</style></notes></record></records></xml>