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BAC CGH array profiling using Phi29-amplified microdissected samples

ABSTRACT: Details of the experiment are available within the Nucleic Acid Research, 2004 manuscript "Genomic profiling by DNA amplification of laser capture microdissected tissues and array CGH", by Cardoso J. et al. Keywords: other

ORGANISM(S): Homo sapiens

PROVIDER: GSE1841 | GEO | 2004/10/23

SECONDARY ACCESSION(S): PRJNA90451

REPOSITORIES: GEO

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BAC CGH array profiling using Phi29-amplified microdissected samples

Project description:Details of the experiment are available within the Nucleic Acid Research, 2004 manuscript "Genomic profiling by DNA amplification of laser capture microdissected tissues and array CGH", by Cardoso J. et al.

2010-06-05 | E-GEOD-1841 | biostudies-arrayexpress

BAC CGH array profiling using Phi29-amplified colon mucosa of microdissected samples from APC and MYH mutation carriers.

Project description:Details of the series are available in the publication Cardoso J. et al., “Chromosomal instability in MYH- and APC-mutant adenomatous polyps”, Cancer Research, accepted for publication. Abstract of the publication: “The vast majority of colorectal cancers display genetic instability, either in the chromosomal (CIN) or microsatellite (MIN) forms. While CIN tumors are per definition aneuploid, MIN colorectal cancers, caused by loss of mismatch repair function, are usually near-diploid. Recently, bi-allelic germline mutations in the MYH gene, were found to be responsible for MAP (MYH associated polyposis), an autosomal recessive predisposition to multiple colorectal polyps, often indistinguishable from the dominant FAP (familial adenomatous polyposis) syndrome caused by inherited APC mutations. Here, we analyzed MYH- and APC-mutant polyps by combining laser-capture microdissection, isothermal genomic DNA amplification, and array-CGH (comparative genomic hybridization). Smoothed quantile regression methods were applied to the MAP and FAP genomic profiles to discriminate chromosomes predominantly affected by gains and losses. Up to 80% of the MAP polyps showed aneuploid changes, which is significantly higher than the 60% found among FAP polyps. Both MAP and FAP adenomas were characterized by frequent losses at chromosome 1p, 17, 19 and 22, and gains affecting chromosome 7 and 13. The observation that aneuploidy is already detectable at early stages of MYH-driven tumorigenesis raises the possibility that CIN may contribute significantly to accelerated tumor progression, increased cancer risk, and poor prognosis in MAP.” Keywords: repeat, BAC, CGH

2005-12-25 | GSE3898 | GEO

BAC CGH array profiling using Phi29-amplified colon mucosa of microdissected samples from APC and MYH mutation carriers.

Project description:Details of the series are available in the publication Cardoso J. et al., âChromosomal instability in MYH- and APC-mutant adenomatous polypsâ, Cancer Research, accepted for publication. Abstract of the publication: âThe vast majority of colorectal cancers display genetic instability, either in the chromosomal (CIN) or microsatellite (MIN) forms. While CIN tumors are per definition aneuploid, MIN colorectal cancers, caused by loss of mismatch repair function, are usually near-diploid. Recently, bi-allelic germline mutations in the MYH gene, were found to be responsible for MAP (MYH associated polyposis), an autosomal recessive predisposition to multiple colorectal polyps, often indistinguishable from the dominant FAP (familial adenomatous polyposis) syndrome caused by inherited APC mutations. Here, we analyzed MYH- and APC-mutant polyps by combining laser-capture microdissection, isothermal genomic DNA amplification, and array-CGH (comparative genomic hybridization). Smoothed quantile regression methods were applied to the MAP and FAP genomic profiles to discriminate chromosomes predominantly affected by gains and losses. Up to 80% of the MAP polyps showed aneuploid changes, which is significantly higher than the 60% found among FAP polyps. Both MAP and FAP adenomas were characterized by frequent losses at chromosome 1p, 17, 19 and 22, and gains affecting chromosome 7 and 13. The observation that aneuploidy is already detectable at early stages of MYH-driven tumorigenesis raises the possibility that CIN may contribute significantly to accelerated tumor progression, increased cancer risk, and poor prognosis in MAP.â Details of the series are available in the publication Cardoso J. et al., âChromosomal instability in MYH- and APC-mutant adenomatous polypsâ, Cancer Research, accepted for publication.

2010-06-30 | E-GEOD-3898 | biostudies-arrayexpress

SADE analysis of microdissected kidney

Project description:SADE analysis of microdissected kidney

| PRJNA87651 | ENA

Genomic profiling by DNA amplification of laser capture microdissected tissues and array CGH.

Project description: Not available

| S-EPMC528818 | biostudies-other

Genome-Wide Gene Dosage Representation in Phi29-Amplified DNA

Project description:Corresponds to Bredel et al 2005 Figure 2 Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set

2006-01-21 | GSE4079 | GEO

Transcription profiling of microdissected human microdissected pancreas ductal adenocarcinoma vs. microdissected normal duct cells

Project description:Comparison of the gene expression of microdissected pancreas ductal adenocarcinoma to microdissected normal duct cells

2006-12-24 | E-MEXP-950 | biostudies-arrayexpress

Gene expression of microdissected colon epithelium

Project description:Gene expression of microdissected colon epithelium

| PRJNA742364 | ENA

Microarray-based CGH using BAC clones

Project description:High resolution BAC array used to study changes in the copy number of chromosome 21 in Acute Meyloid Leukemia patients Genomic DNA from patients as well as from normal donors were differentially labelled and hybridized on the array 36 RPCI-11 BAC clones covering the q-arm of chromosome21 from position15.1MB(close to the centromere)to the telomeric position 46.9 MB with an average gap between clones of 800 kb (range 346-1593 kb)In addition 23 randomly selected clones, each representing 1 of the remaining chromosomes1-20,22,X and YPositions of genes and BAC clones were determined according to the NCBI (http://www.ncbi.nlm.nih.gov/mapview) 59 BAC clones spotted in 6 replicas for a total 354 spots on GAPII corning glass slides using Affymetrix GMS417 Affymetrix Arrayer with 4-ring&pin configuration. (Affymetrix,Santa Clara, CA). Purified clones spotted in 50%DMSO DNA Isolation of these clones was performed from bacterial culture (250ml) using Qiagen midi kit (Qiagen, Valencia CA) gDNA from AML patients and healthy controls was extracted and labelleb according to the published protocol by JR Pollack in Nature Genetics vol.23 Sep.99, also available http://cmgm.stanford.edu/pbrown/protocols/4_genomic.html Fluorescence intensity ratios were measured in control experiments (reference versus reference hybridization) to weight DNA Amplification or deletion Fluorescence ratio >1 indicates amplification, Fluorescence ratio <1 indicate deletion Mean of the background corrected pixel-by-pixel fluorescence ratio between the two dyes at each spot was obtained by genePix software. Series_platform_id: my_array13 Series_submitter weblink: www.dnaarrays.org Keywords: other

2004-02-29 | GSE1078 | GEO

Genome-Wide Gene Dosage Representation in Phi29-Amplified DNA

Project description:Corresponds to Bredel et al 2005 Figure 2 Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Using regression correlation

2006-01-20 | E-GEOD-4079 | biostudies-arrayexpress

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