Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA136835 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Purpose: To improve clinical outcome of gastric cancer patients, most emphasis is on improving therapeutic regimens, including more extensive surgery as well as (neo)adjuvant chemotherapy. The present study set out to identify, based on DNA copy number profiling, subgroups of patients with different clinical outcomes who thus would qualify for different therapy intensities. Experimental Design: DNA of 206 gastric cancer patients was isolated and analyzed by genome wide array comparative genomic hybridization. DNA copy number profiles were evaluated and correlated to lymph node status and survival. In addition, HSP90 protein expression was analyzed and correlated to survival in 290 gastric cancer patients. Results: Frequent (>20%) DNA copy number gains were observed on chromosomes 1p, 6p, 7p, 7q, 8q, 11q, 12q, 13q, 16p, 16q, 17q, 19p, 19q, 20p, 20q, 21q and 22q, and losses on chromosomes 4p, 4q, 6p, 6q, 9p, 13q and 21q. Lymph node negative gastric cancers showed significantly more losses on chromosomes 5q11.2-q35.1, 10q11.23-21.3 and 14q32.11-q32.33. In addition, losses on 5q11.2-q31.3 and 14q32.11-q32.33 were highly correlated to good clinical outcome, in both lymph node negative and positive gastric cancer patients. Loss of expression of HSP90, located on chromosome 14q32.2, correlated to good survival time. Conclusion: Genome wide DNA copy number profiling allows to identify a subgroup of gastric cancers, marked by losses on chromosomes 5q11.2-q31.3 and 14q32.11-q32.33 that have an excellent clinical outcome after surgery alone, and patients with these tumors are unlikely to benefit from additional intensified therapies. Possible biological mechanisms could involve loss of heat shock proteins, of which the coding genes are located at these chromosomal regions. 183 gastric adenocarcinomas
2012-05-09 | E-GEOD-26389 | biostudies-arrayexpress
Project description:Purpose: To improve clinical outcome of gastric cancer patients, most emphasis is on improving therapeutic regimens, including more extensive surgery as well as (neo)adjuvant chemotherapy. The present study set out to identify, based on DNA copy number profiling, subgroups of patients with different clinical outcomes who thus would qualify for different therapy intensities. Experimental Design: DNA of 206 gastric cancer patients was isolated and analyzed by genome wide array comparative genomic hybridization. DNA copy number profiles were evaluated and correlated to lymph node status and survival. In addition, HSP90 protein expression was analyzed and correlated to survival in 290 gastric cancer patients. Results: Frequent (>20%) DNA copy number gains were observed on chromosomes 1p, 6p, 7p, 7q, 8q, 11q, 12q, 13q, 16p, 16q, 17q, 19p, 19q, 20p, 20q, 21q and 22q, and losses on chromosomes 4p, 4q, 6p, 6q, 9p, 13q and 21q. Lymph node negative gastric cancers showed significantly more losses on chromosomes 5q11.2-q35.1, 10q11.23-21.3 and 14q32.11-q32.33. In addition, losses on 5q11.2-q31.3 and 14q32.11-q32.33 were highly correlated to good clinical outcome, in both lymph node negative and positive gastric cancer patients. Loss of expression of HSP90, located on chromosome 14q32.2, correlated to good survival time. Conclusion: Genome wide DNA copy number profiling allows to identify a subgroup of gastric cancers, marked by losses on chromosomes 5q11.2-q31.3 and 14q32.11-q32.33 that have an excellent clinical outcome after surgery alone, and patients with these tumors are unlikely to benefit from additional intensified therapies. Possible biological mechanisms could involve loss of heat shock proteins, of which the coding genes are located at these chromosomal regions.
2012-05-10 | GSE26389 | GEO
Project description:The aim of this study is to establish an integrative profiling of recurrent UPDs/UPPs, CNAs and genome-wide methylation status in sporadic CRC. Our results indicate that regions showing high frequencies of UPDs/UPPs mostly coincide with regions typically involved in genomic losses such as chromosome arms 1p, 5q, 8p, 14q, 17p, 18q, 20p, and 22q. Of these, chromosome arms 5q, 14q, 17p, and 20p preferentially showed UPDs/UPPs over genomic losses suggesting that tumor cells must maintain the disomic state of certain genes to favor cellular fitness. A meta-analysis using over 300 samples from The Cancer Genome Atlas confirmed our findings. In addition, the genes CSPG2, FLT4, SFRP1, DLK1, and GAS7 were frequently involved in regions of UPDs/UPPs and showed high levels of methylation revealing that UPDs/UPPs can result in the duplication of hypermethylated inactive genes. A total of 32 primary tumors from the colon and rectum were collected from the Hospital Clinic of Barcelona under the supervision of an experienced pathologist. DNA was extracted and bisulfited according to manufacturer's protocols. Matched patient DNA from normal mucosa was used as a reference for these experiments. This dataset includes methylation data for 29 colorectal cancers (only including those with good QC).
2015-09-02 | E-GEOD-64112 | biostudies-arrayexpress
Project description:The biological behavior and clinical outcome of gastric cancers are variable considerably according to anatomic location, such as proximal gastric cancer (PGC) and distal gastric cancer (DGC). Therefore, identification of the biomarkers used for recognizing the biological behavior and predicting clinical outcome has been a major goal in gastric cancer researches.
2013-03-27 | E-MTAB-1307 | biostudies-arrayexpress
Project description:The aim of this study is to establish an integrative profiling of recurrent UPDs/UPPs, CNAs and genome-wide methylation status in sporadic CRC. Our results indicate that regions showing high frequencies of UPDs/UPPs mostly coincide with regions typically involved in genomic losses such as chromosome arms 1p, 5q, 8p, 14q, 17p, 18q, 20p, and 22q. Of these, chromosome arms 5q, 14q, 17p, and 20p preferentially showed UPDs/UPPs over genomic losses suggesting that tumor cells must maintain the disomic state of certain genes to favor cellular fitness. A meta-analysis using over 300 samples from The Cancer Genome Atlas confirmed our findings. In addition, the genes CSPG2, FLT4, SFRP1, DLK1, and GAS7 were frequently involved in regions of UPDs/UPPs and showed high levels of methylation revealing that UPDs/UPPs can result in the duplication of hypermethylated inactive genes. This dataset includes the array CGH of 30 colorectal cancers.
2015-09-02 | GSE64110 | GEO
Project description:The aim of this study is to establish an integrative profiling of recurrent UPDs/UPPs, CNAs and genome-wide methylation status in sporadic CRC. Our results indicate that regions showing high frequencies of UPDs/UPPs mostly coincide with regions typically involved in genomic losses such as chromosome arms 1p, 5q, 8p, 14q, 17p, 18q, 20p, and 22q. Of these, chromosome arms 5q, 14q, 17p, and 20p preferentially showed UPDs/UPPs over genomic losses suggesting that tumor cells must maintain the disomic state of certain genes to favor cellular fitness. A meta-analysis using over 300 samples from The Cancer Genome Atlas confirmed our findings. In addition, the genes CSPG2, FLT4, SFRP1, DLK1, and GAS7 were frequently involved in regions of UPDs/UPPs and showed high levels of methylation revealing that UPDs/UPPs can result in the duplication of hypermethylated inactive genes. This dataset includes the array CGH of 30 colorectal cancers.
2015-09-02 | GSE64109 | GEO
Project description:The aim of this study is to establish an integrative profiling of recurrent UPDs/UPPs, CNAs and genome-wide methylation status in sporadic CRC. Our results indicate that regions showing high frequencies of UPDs/UPPs mostly coincide with regions typically involved in genomic losses such as chromosome arms 1p, 5q, 8p, 14q, 17p, 18q, 20p, and 22q. Of these, chromosome arms 5q, 14q, 17p, and 20p preferentially showed UPDs/UPPs over genomic losses suggesting that tumor cells must maintain the disomic state of certain genes to favor cellular fitness. A meta-analysis using over 300 samples from The Cancer Genome Atlas confirmed our findings. In addition, the genes CSPG2, FLT4, SFRP1, DLK1, and GAS7 were frequently involved in regions of UPDs/UPPs and showed high levels of methylation revealing that UPDs/UPPs can result in the duplication of hypermethylated inactive genes. This dataset includes the array CGH of 30 colorectal cancers. A total of 30 primary tumors from the colon and rectum were collected from the Hospital Clinic of Barcelona under the supervision of an experienced pathologist. DNA was extracted and labeled according to manufacturer's protocols. Matched patient DNA from normal mucosa was used as a reference for these experiments.
2015-09-02 | E-GEOD-64110 | biostudies-arrayexpress
Project description:The aim of this study is to establish an integrative profiling of recurrent UPDs/UPPs, CNAs and genome-wide methylation status in sporadic CRC. Our results indicate that regions showing high frequencies of UPDs/UPPs mostly coincide with regions typically involved in genomic losses such as chromosome arms 1p, 5q, 8p, 14q, 17p, 18q, 20p, and 22q. Of these, chromosome arms 5q, 14q, 17p, and 20p preferentially showed UPDs/UPPs over genomic losses suggesting that tumor cells must maintain the disomic state of certain genes to favor cellular fitness. A meta-analysis using over 300 samples from The Cancer Genome Atlas confirmed our findings. In addition, the genes CSPG2, FLT4, SFRP1, DLK1, and GAS7 were frequently involved in regions of UPDs/UPPs and showed high levels of methylation revealing that UPDs/UPPs can result in the duplication of hypermethylated inactive genes. This dataset includes the array CGH of 30 colorectal cancers. A total of 30 primary tumors from the colon and rectum were collected from the Hospital Clinic of Barcelona under the supervision of an experienced pathologist. DNA was extracted and labeled according to manufacturer's protocols. Matched patient DNA from normal mucosa was used as a reference for these experiments.
2015-09-02 | E-GEOD-64109 | biostudies-arrayexpress
Project description:The aim of this study is to establish an integrative profiling of recurrent UPDs/UPPs, CNAs and genome-wide methylation status in sporadic CRC. Our results indicate that regions showing high frequencies of UPDs/UPPs mostly coincide with regions typically involved in genomic losses such as chromosome arms 1p, 5q, 8p, 14q, 17p, 18q, 20p, and 22q. Of these, chromosome arms 5q, 14q, 17p, and 20p preferentially showed UPDs/UPPs over genomic losses suggesting that tumor cells must maintain the disomic state of certain genes to favor cellular fitness. A meta-analysis using over 300 samples from The Cancer Genome Atlas confirmed our findings. In addition, the genes CSPG2, FLT4, SFRP1, DLK1, and GAS7 were frequently involved in regions of UPDs/UPPs and showed high levels of methylation revealing that UPDs/UPPs can result in the duplication of hypermethylated inactive genes.
2015-09-02 | GSE64112 | GEO
Project description:Hypothesis: Non-small cell lung cancer (NSCLC) is characterized by a multitude of genetic aberrations with unknown clinical impact. In this study, we aimed to identify gene copy number changes that correlate with clinical outcome in NSCLC. To maximize the chance to identify clinically relevant events, we applied a strategy involving two prognostically extreme patient groups. Results: Genetic aberrations were strongly associated with tumor histology. In adenocarcinoma (n=50), gene copy number gains on chromosome 8q21-q24.3 (177 genes) were more frequent in long-term survivors. In squamous cell carcinoma (n=28), gains on chromosome 14q23.1-24.3 (133 genes) were associated with shorter survival, whereas losses in a neighboring region, 14q31.1-32.33 (110 genes), correlated with favorable outcome. In accordance with copy number gains and losses, mRNA expression levels of corresponding genes were increased or decreased, respectively. Conclusion: Comprehensive tumor profiling permits the integration of genomic, histologic and clinical data. We identified gene copy number gains and losses, with corresponding changes in mRNA levels, that were associated with prognosis in adenocarcinoma and squamous cell carcinoma of the lung.
2011-11-01 | GSE28572 | GEO