<?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%">Cascon, A.</style></author><author><style face="normal" font="default" size="100%">Ruiz-Llorente, S.</style></author><author><style face="normal" font="default" size="100%">Rodriguez-Perales, S.</style></author><author><style face="normal" font="default" size="100%">Honrado, E.</style></author><author><style face="normal" font="default" size="100%">Martinez-Ramirez, A.</style></author><author><style face="normal" font="default" size="100%">Leton, R.</style></author><author><style face="normal" font="default" size="100%">Montero-Conde, C.</style></author><author><style face="normal" font="default" size="100%">Benitez, J.</style></author><author><style face="normal" font="default" size="100%">Dopazo, J.</style></author><author><style face="normal" font="default" size="100%">Cigudosa, J. C.</style></author><author><style face="normal" font="default" size="100%">M. Robledo</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">A novel candidate region linked to development of both pheochromocytoma and head/neck paraganglioma</style></title><secondary-title><style face="normal" font="default" size="100%">Genes Chromosomes Cancer</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">80 and over Child Chromosomes</style></keyword><keyword><style  face="normal" font="default" size="100%">Adolescent Adrenal Gland Neoplasms/*genetics Adult Aged Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Biological/*genetics</style></keyword><keyword><style  face="normal" font="default" size="100%">Human</style></keyword><keyword><style  face="normal" font="default" size="100%">Pair 1/genetics Chromosomes</style></keyword><keyword><style  face="normal" font="default" size="100%">Pair 11/genetics Chromosomes</style></keyword><keyword><style  face="normal" font="default" size="100%">Pair 3/genetics Chromosomes</style></keyword><keyword><style  face="normal" font="default" size="100%">Pair 8/genetics Female Gene Deletion Head and Neck Neoplasms/*genetics Humans Male Middle Aged Nucleic Acid Hybridization Paraganglioma/*genetics Pheochromocytoma/*genetics Tumor Markers</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=15609347</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">3</style></number><volume><style face="normal" font="default" size="100%">42</style></volume><pages><style face="normal" font="default" size="100%">260-8</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Although the histologic distinction between pheochromocytomas and head and neck paragangliomas is clear, little is known about the genetic differences between them. To date, various sets of genes have been found to be involved in inherited susceptibility to developing both tumor types, but the genes involved in sporadic pathogenesis are still unknown. To define new candidate regions, we performed CGH analysis on 29 pheochromocytomas and on 24 paragangliomas mainly of head and neck origin (20 of 24), which allowed us to differentiate between the two tumor types. Loss of 3q was significantly more frequent in pheochromocytomas, and loss of 1q appeared only in paragangliomas. We also found gain of 11q13 to be a significantly frequent alteration in malignant cases of both types. In addition, recurrent loss of 8p22-23 was found in 62% of pheochromocytomas (including all malignant cases) versus in 33% of paragangliomas, suggesting that this region contains candidate genes involved in the pathogenesis of this abnormality. Using FISH analysis on tissue microarrays, we confirmed genomic deletion of this region in 55% of pheochromocytomas compared to 12% of paragangliomas. Loss of 8p22-23 appears to be an important event in the sporadic development of these tumors, and additional molecular studies are necessary to identify candidate genes in this chromosomal region.</style></abstract><notes><style face="normal" font="default" size="100%">Cascon, Alberto Ruiz-Llorente, Sergio Rodriguez-Perales, Sandra Honrado, Emiliano Martinez-Ramirez, Angel Leton, Rocio Montero-Conde, Cristina Benitez, Javier Dopazo, Joaquin Cigudosa, Juan C Robledo, Mercedes Research Support, Non-U.S. Gov’t United States Genes, chromosomes &amp; cancer Genes Chromosomes Cancer. 2005 Mar;42(3):260-8.</style></notes></record><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><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%">Melendez, B.</style></author><author><style face="normal" font="default" size="100%">Diaz-Uriarte, R.</style></author><author><style face="normal" font="default" size="100%">Cuadros, M.</style></author><author><style face="normal" font="default" size="100%">Martinez-Ramirez, A.</style></author><author><style face="normal" font="default" size="100%">Fernandez-Piqueras, J.</style></author><author><style face="normal" font="default" size="100%">Dopazo, A.</style></author><author><style face="normal" font="default" size="100%">Cigudosa, J. C.</style></author><author><style face="normal" font="default" size="100%">Rivas, C.</style></author><author><style face="normal" font="default" size="100%">Dopazo, J.</style></author><author><style face="normal" font="default" size="100%">Martinez-Delgado, B.</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%">Gene expression analysis of chromosomal regions with gain or loss of genetic material detected by comparative genomic hybridization</style></title><secondary-title><style face="normal" font="default" size="100%">Genes Chromosomes Cancer</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Chromosomes</style></keyword><keyword><style  face="normal" font="default" size="100%">Fluorescence Lymphoma</style></keyword><keyword><style  face="normal" font="default" size="100%">Human</style></keyword><keyword><style  face="normal" font="default" size="100%">Pair 13/*genetics Chromosomes</style></keyword><keyword><style  face="normal" font="default" size="100%">Pair 19/*genetics Chromosomes</style></keyword><keyword><style  face="normal" font="default" size="100%">Pair 6/*genetics Expressed Sequence Tags *Gene Dosage Gene Expression Profiling Humans In Situ Hybridization</style></keyword><keyword><style  face="normal" font="default" size="100%">T-Cell/*genetics Nucleic Acid Hybridization Oligonucleotide Array Sequence Analysis</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2004</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=15382261</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">4</style></number><volume><style face="normal" font="default" size="100%">41</style></volume><pages><style face="normal" font="default" size="100%">353-65</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Comparative genomic hybridization (CGH) has been widely used to detect copy number alterations in cancer and to identify regions containing candidate tumor-responsible genes; however, gene expression changes have been described only in highly amplified regions (amplicons). To study the overall impact of slight copy number changes on gene expression, we analyzed 16 T-cell lymphomas by using CGH and a custom-designed cDNA microarray containing 7,657 genes and expressed sequence tags related to tumorigenesis. We evaluated mean gene expression and variability within CGH-altered regions and explored the relationship between the effects of the gene and its position within these regions. Minimally overlapping CGH candidate areas (6q25, 13q21-q22, and 19q13.1) revealed a weak relationship between altered genomic content and gene expression. However, some candidate genes showed modified expression within these regions in the majority of tumors; these candidate genes were evaluated and confirmed in another independent series of 23 T-cell lymphomas by use of the same cDNA microarray and by FISH on a tissue microarray. When all the CGH regions detected for each tumor were considered, we found a significant increase or decrease in the mean expression of the genes contained in gained or lost regions, respectively. In addition, we found that the expression of a gene was dependent not only on its position within an altered region but also on its own mechanism of regulation: genes in the same altered region responded very differently to the gain or loss of genetic material. Supplementary material for this article can be found on the Genes, Chromosomes, and Cancer website at http://www.interscience.wiley.com/jpages/1045-2257/suppmat/index.html.</style></abstract><notes><style face="normal" font="default" size="100%">Melendez, Barbara Diaz-Uriarte, Ramon Cuadros, Marta Martinez-Ramirez, Angel Fernandez-Piqueras, Jose Dopazo, Ana Cigudosa, Juan-Cruz Rivas, Carmen Dopazo, Joaquin Martinez-Delgado, Beatriz Benitez, Javier Research Support, Non-U.S. Gov’t United States Genes, chromosomes &amp; cancer Genes Chromosomes Cancer. 2004 Dec;41(4):353-65.</style></notes></record></records></xml>