@article {15709182,
	title = {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},
	journal = {Clin Cancer Res},
	volume = {11},
	number = {3},
	year = {2005},
	note = {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{\textquoteright}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.},
	pages = {1146-53},
	abstract = {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 >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 >50\%. Interestingly, 84.6\% of the cases (11 of 13) assigned to the BRCA1 class with a probability >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.},
	keywords = {BRCA1 Protein/*genetics BRCA2 Protein/*genetics Breast Neoplasms/*genetics/pathology Chromosomes, Genetic/*genetics, Human, Human Humans Male Mutation Nucleic Acid Hybridization/methods Promoter Regions, Pair 12/genetics Chromosomes, Pair 15/genetics Chromosomes, Pair 18/genetics Chromosomes, Pair 2/genetics Chromosomes, Pair 8/genetics *DNA Methylation Female Genome},
	url = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve\&db=PubMed\&dopt=Citation\&list_uids=15709182},
	author = {Alvarez, S. and Diaz-Uriarte, R. and Osorio, A. and Barroso, A. and Melchor, L. and Paz, M. F. and Honrado, E. and Rodriguez, R. and Urioste, M. and Valle, L. and Diez, O. and Cigudosa, J. C. and Dopazo, J. and Esteller, M. and Benitez, J.}
}
@article {15382261,
	title = {Gene expression analysis of chromosomal regions with gain or loss of genetic material detected by comparative genomic hybridization},
	journal = {Genes Chromosomes Cancer},
	volume = {41},
	number = {4},
	year = {2004},
	note = {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{\textquoteright}t United States Genes, chromosomes \& cancer Genes Chromosomes Cancer. 2004 Dec;41(4):353-65.},
	pages = {353-65},
	abstract = {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.},
	keywords = {Chromosomes, Fluorescence Lymphoma, Human, Pair 13/*genetics Chromosomes, Pair 19/*genetics Chromosomes, Pair 6/*genetics Expressed Sequence Tags *Gene Dosage Gene Expression Profiling Humans In Situ Hybridization, T-Cell/*genetics Nucleic Acid Hybridization Oligonucleotide Array Sequence Analysis},
	url = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve\&db=PubMed\&dopt=Citation\&list_uids=15382261},
	author = {Melendez, B. and Diaz-Uriarte, R. and Cuadros, M. and Martinez-Ramirez, A. and Fernandez-Piqueras, J. and Dopazo, A. and Cigudosa, J. C. and Rivas, C. and Dopazo, J. and Martinez-Delgado, B. and Benitez, J.}
}
