<?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%">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><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%">Tracey, L.</style></author><author><style face="normal" font="default" size="100%">Villuendas, R.</style></author><author><style face="normal" font="default" size="100%">Ortiz, P.</style></author><author><style face="normal" font="default" size="100%">Dopazo, A.</style></author><author><style face="normal" font="default" size="100%">Spiteri, I.</style></author><author><style face="normal" font="default" size="100%">Lombardia, L.</style></author><author><style face="normal" font="default" size="100%">Rodriguez-Peralto, J. L.</style></author><author><style face="normal" font="default" size="100%">Fernandez-Herrera, J.</style></author><author><style face="normal" font="default" size="100%">Hernandez, A.</style></author><author><style face="normal" font="default" size="100%">Fraga, J.</style></author><author><style face="normal" font="default" size="100%">Dominguez, O.</style></author><author><style face="normal" font="default" size="100%">Herrero, J.</style></author><author><style face="normal" font="default" size="100%">Alonso, M. A.</style></author><author><style face="normal" font="default" size="100%">Dopazo, J.</style></author><author><style face="normal" font="default" size="100%">Piris, M. A.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Identification of genes involved in resistance to interferon-alpha in cutaneous T-cell lymphoma</style></title><secondary-title><style face="normal" font="default" size="100%">Am J Pathol</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Antineoplastic Agents/*pharmacology/therapeutic use Carrier Proteins/biosynthesis/genetics DNA-Binding Proteins/biosynthesis/genetics Drug Resistance</style></keyword><keyword><style  face="normal" font="default" size="100%">Biological Oligonucleotide Array Sequence Analysis RNA</style></keyword><keyword><style  face="normal" font="default" size="100%">Cultured</style></keyword><keyword><style  face="normal" font="default" size="100%">Cutaneous/diagnosis/drug therapy/*genetics/metabolism *Membrane Glycoproteins Models</style></keyword><keyword><style  face="normal" font="default" size="100%">Interleukin-1 Reproducibility of Results STAT1 Transcription Factor STAT3 Transcription Factor Trans-Activators/biosynthesis/genetics Tumor Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Neoplasm Gene Expression Profiling *Gene Expression Regulation</style></keyword><keyword><style  face="normal" font="default" size="100%">Neoplasm/biosynthesis *Receptors</style></keyword><keyword><style  face="normal" font="default" size="100%">Neoplastic Humans Interferon-alpha/*pharmacology/therapeutic use Kinetics Lymphoma</style></keyword><keyword><style  face="normal" font="default" size="100%">T-Cell</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2002</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=12414529</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">5</style></number><volume><style face="normal" font="default" size="100%">161</style></volume><pages><style face="normal" font="default" size="100%">1825-37</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Interferon-alpha therapy has been shown to be active in the treatment of mycosis fungoides although the individual response to this therapy is unpredictable and dependent on essentially unknown factors. In an effort to better understand the molecular mechanisms of interferon-alpha resistance we have developed an interferon-alpha resistant variant from a sensitive cutaneous T-cell lymphoma cell line. We have performed expression analysis to detect genes differentially expressed between both variants using a cDNA microarray including 6386 cancer-implicated genes. The experiments showed that resistance to interferon-alpha is consistently associated with changes in the expression of a set of 39 genes, involved in signal transduction, apoptosis, transcription regulation, and cell growth. Additional studies performed confirm that STAT1 and STAT3 expression and interferon-alpha induction and activation are not altered between both variants. The gene MAL, highly overexpressed by resistant cells, was also found to be expressed by tumoral cells in a series of cutaneous T-cell lymphoma patients treated with interferon-alpha and/or photochemotherapy. MAL expression was associated with longer time to complete remission. Time-course experiments of the sensitive and resistant cells showed a differential expression of a subset of genes involved in interferon-response (1 to 4 hours), cell growth and apoptosis (24 to 48 hours.), and signal transduction.</style></abstract><notes><style face="normal" font="default" size="100%">Tracey, Lorraine Villuendas, Raquel Ortiz, Pablo Dopazo, Ana Spiteri, Inmaculada Lombardia, Luis Rodriguez-Peralto, Jose L Fernandez-Herrera, Jesus Hernandez, Almudena Fraga, Javier Dominguez, Orlando Herrero, Javier Alonso, Miguel A Dopazo, Joaquin Piris, Miguel A Research Support, Non-U.S. Gov’t United States The American journal of pathology Am J Pathol. 2002 Nov;161(5):1825-37.</style></notes></record></records></xml>