Gene Abnormality in colorectal cancers from kashmir
Ontology highlight
ABSTRACT:
DISEASE(S): Patients With Colon Or Rectal Malignancy
PROVIDER: 2576008 | ecrin-mdr-crc |
REPOSITORIES: ECRIN MDR
Similar Datasets
Project description:Wiskott-Aldrich syndrome (WAS) predisposes patients to leukemia and lymphoma. WAS is caused by mutations in the protein WASP which impair its interaction with the WIPF1 protein. Here, we aim to identify a module of WIPF1-coexpressed genes and to assess its use as a prognostic signature for colorectal cancer, glioma, and breast cancer patients. Two public colorectal cancer microarray data sets were used for discovery and validation of the WIPF1 co-expression module. Based on expression of the WIPF1 signature, we classified more than 400 additional tumors with microarray data from our own experiments or from publicly available data sets according to their WIPF1 signature expression. This allowed us to separate patient populations for colorectal cancers, breast cancers, and gliomas for which clinical characteristics like survival times and times to relapse were analyzed. Groups of colorectal cancer, breast cancer, and glioma patients with low expression of the WIPF1 co-expression module generally had a favorable prognosis. In addition, the majority of WIPF1 signature genes are individually correlated with disease outcome in different studies. Literature gene network analysis revealed that among WIPF1 co-expressed genes known direct transcriptional targets of c-myc, ESR1 and p53 are enriched. The mean expression profile of WIPF1 signature genes is correlated with the profile of a proliferation signature. The WIPF1 signature is the first microarray-based prognostic expression signature primarily developed for colorectal cancer that is instrumental in other tumor types: low expression of the WIPF1 module is associated with better prognosis. We used microarrays for the validation of a WIPF1 co-expression module which was developed on two publically available datasets. Keywords: disease state analysis For the generation of our own microarray data set, 62 CRC patients undergoing elective standard oncological resection at the Department of General, Vascular and Thoracic Surgery, Campus Benjamin Franklin, Charité, were prospectively recruited.
2009-05-04 | E-GEOD-12945 | biostudies-arrayexpress
Project description:Copy number analyses of regionally separated biopsies from primary and metastatic lesions of five colorectal cancers A total of 35 intratumoral biopsies were obtained from primary and metastatic lesions of five colorectal cancers. Board-certified pathologists reviewed the hematoxylin&eosin stained sections and identified tumor-rich regions (> 80% purity) to ensure minimal contamination of normal tissues. We selected two to six different areas for biopsy that were at least 5mm apart in primary and distant metastatic lesions from a same patient. Copy number profiling was performed using Agilent 180K platform according to the manufacturer's protocol. The genomic DNA obtained from the adjacent normal tissues were used as reference genomic DNA for the tumor DNA of the corresponding patients.
2014-06-16 | E-GEOD-58512 | biostudies-arrayexpress
Project description:Wiskott-Aldrich syndrome (WAS) predisposes patients to leukemia and lymphoma. WAS is caused by mutations in the protein WASP which impair its interaction with the WIPF1 protein. Here, we aim to identify a module of WIPF1-coexpressed genes and to assess its use as a prognostic signature for colorectal cancer, glioma, and breast cancer patients. Two public colorectal cancer microarray data sets were used for discovery and validation of the WIPF1 co-expression module. Based on expression of the WIPF1 signature, we classified more than 400 additional tumors with microarray data from our own experiments or from publicly available data sets according to their WIPF1 signature expression. This allowed us to separate patient populations for colorectal cancers, breast cancers, and gliomas for which clinical characteristics like survival times and times to relapse were analyzed. Groups of colorectal cancer, breast cancer, and glioma patients with low expression of the WIPF1 co-expression module generally had a favorable prognosis. In addition, the majority of WIPF1 signature genes are individually correlated with disease outcome in different studies. Literature gene network analysis revealed that among WIPF1 co-expressed genes known direct transcriptional targets of c-myc, ESR1 and p53 are enriched. The mean expression profile of WIPF1 signature genes is correlated with the profile of a proliferation signature. The WIPF1 signature is the first microarray-based prognostic expression signature primarily developed for colorectal cancer that is instrumental in other tumor types: low expression of the WIPF1 module is associated with better prognosis. We used microarrays for the validation of a WIPF1 co-expression module which was developed on two publically available datasets. Keywords: disease state analysis
2009-05-04 | GSE12945 | GEO
Project description:Copy number analyses of regionally separated biopsies from primary and metastatic lesions of five colorectal cancers
2014-06-16 | GSE58512 | GEO
Project description:Gene expression data from colorectal cancers
| PRJNA417177 | ENA
Project description:Samples were taken from colorectal cancers in surgically resected specimens in 155 colorectal cancer patients. The expression profiles were determined using Affymetrix Human Genome U133Plus 2.0 arrays. Our MSI/MSS classifier was applied to these samples. Experiment Overall Design: mRNA from one-hundred-fifty-five primary colorectal tumour samples were extracted and hybridized to HG-U133Plus 2.0 expression arrays. The MAS5.0 procedure was used to make calls of expression. Data from each sample were quantile normalized and log-2 transformed.
2009-02-07 | E-GEOD-13294 | biostudies-arrayexpress
Project description:To investigate the genetic relationship between two major grain length loci GS3 and qGL3, we developed the near-isogenic lines (NILs), NIL-GS3 (GS3/qGL3), NIL-qgl3 (gs3/qgl3), NIL-GS3/qgl3 (GS3/qgl3) in the background of 93-11 (gs3/qGL3) by crossing and MAS approach. Four samples was analyzed: three near-isogenic lines (NILs), NIL-GS3 (GS3/qGL3), NIL-qgl3 (gs3/qgl3), NIL-GS3/qgl3 (GS3/qgl3) and their background of 93-11. Every sample had three independed duplications. And the primary panicle with 3-6 cm length from the three NILs and 93-11 were used for RNA preparation and hybrid with Rice Genome OneArray Microarray (Phalanx Biotech Group).
2014-07-22 | E-GEOD-59619 | biostudies-arrayexpress
Project description:Samples were taken from colorectal cancers in surgically resected specimens from 74 patients. The expression profiles were determined using Affymetrix Human Genome U133Plus 2.0 arrays. Our MSI/MSS classifer was applied to these samples. Experiment Overall Design: mRNA from 74 fresh-frozen primary colorectal tumour samples were extracted and hybridized to HG-U133Plus 2.0 expression arrays. The MAS5.0 procedure was used to make calls of expression. Data from each sample were quantile normalized with reference to a training set prior to application of our MSS/MSI classifier.
2009-01-16 | E-GEOD-13067 | biostudies-arrayexpress
Project description:Comparison of genomic alterations of primary colorectal cancers with liver metastases of the same patient Keywords: array CGH, colorectal cancer, colon cancer, liver metastasis 21 primary colorectal cancers and 21 matched liver metastases hybridized against sex-matched control pools
2010-07-07 | E-GEOD-10179 | biostudies-arrayexpress
Project description:D122p53 mice (a model of D133p53 isoform) are tumour prone, have extensive inflammation and elevated serum IL-6. To investigate the role of IL-6 we crossed ∆122p53 mice with IL-6 deficient mice. Here we show that loss of IL-6 reduced JAK-STAT signalling, tumour incidence, and metastasis. We also show that D122p53 activates RhoA-ROCK signalling leading to tumour cell invasion which is IL-6 dependent and can be reduced by inhibition of JAK-STAT and RhoA-ROCK pathways. Similarly, we show that Δ133p53 activates the these pathways, resulting in invasive and migratory phenotypes, in colorectal cancer cells. Gene expression analysis of colorectal tumours showed enrichment of GPCR signalling associated with D133TP53 mRNA. Patients with elevated D133TP53 mRNA levels had a shorter disease free survival. Our results suggest that D133p53 promotes tumour invasion by activation of the JAK-STAT and RhoA-ROCK pathways and that patients whose tumours have high D133p53 may benefit from therapies targeting these pathways. In this dataset, we included the gene expression data from 35 colorectal cancers. These data were used to identify a list of enriched genesets associated with D133TP53 mRNA expression in colorectal tumours
2018-02-14 | GSE106535 | GEO