Identification of subsets of urothelial carcinoma
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Woonyoung Choi
PROVIDER: E-GEOD-48075 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Smoking is a major risk factor for Urothelial carcinoma (UC). However the complex mechanisms, how smoking promotes carcinogenesis and tumour progression, remain obscure. A microarray based approached was therefore performed to detect the smoking derived gene expression alteration in non-malignant and malignant urothelial tissues from patients with superficial or invasive UC. Smoking enhanced cell migration and response to tissue damages. In non-malignant tissues smoking induced immune response and altered the cytoskeleton. In urothelial carcinoma, smoking altered extracellular and chromosome structures. Smoking affected tissues from patients with invasive carcinomamore strongly, up-regulating particularly growth factors and oncogenes in non-malignant tissue of patients with invasive but not with superficial carcinoma. In former smokers, comparable changes were seen in tissues form patients with invasive disease while they were minor or reversed in tissue of patients with superficial disease. Best but not complete tissue repair was suggestedfor non-malignant tissue from patients with superficial tumours. we used microarray techniques to define gene expression profile which may explain the contribution of smoking to urothelial carcinoma. Gene expression profiling using GeneChip HG-U133A Plus 2.0 (Affymetrix) was performed on non-malignant and carcinogenic urothelium from six patients with superficial and six with invasive urothelial carcinoma, each group including two current, former, and non-smokers.
2013-03-20 | E-GEOD-21142 | biostudies-arrayexpress
Project description:Identification of bladder cancer subsets 128 FFPE bladder tumors were used to validate the bladder cancer subsets
2014-02-10 | E-GEOD-48276 | biostudies-arrayexpress
Project description:Bladder cancer tissue from 11 patients diagnosed as superficial and muscle invasive and 7 normal bladder mucoa were analyzed by protein antibody array kit with 656 antibodies
2015-06-11 | GSE69736 | GEO
Project description:Smoking is a major risk factor for Urothelial carcinoma (UC). However the complex mechanisms, how smoking promotes carcinogenesis and tumour progression, remain obscure. A microarray based approached was therefore performed to detect the smoking derived gene expression alteration in non-malignant and malignant urothelial tissues from patients with superficial or invasive UC. Smoking enhanced cell migration and response to tissue damages. In non-malignant tissues smoking induced immune response and altered the cytoskeleton. In urothelial carcinoma, smoking altered extracellular and chromosome structures. Smoking affected tissues from patients with invasive carcinomamore strongly, up-regulating particularly growth factors and oncogenes in non-malignant tissue of patients with invasive but not with superficial carcinoma. In former smokers, comparable changes were seen in tissues form patients with invasive disease while they were minor or reversed in tissue of patients with superficial disease. Best but not complete tissue repair was suggestedfor non-malignant tissue from patients with superficial tumours. we used microarray techniques to define gene expression profile which may explain the contribution of smoking to urothelial carcinoma.
2013-03-20 | GSE21142 | GEO
Project description:Using Affymetrix microarray technology we analyzed the gene expression profiles of the most important pathological categories of bladder cancer in order to detect potential marker genes. Applying an unsupervised cluster algorithm we observed clear differences between tumor and control samples, as well as between superficial and muscle invasive tumors. According to cluster results, the T1 high grade tumor type presented a global genetic profile which could not be distinguished from invasive cases. We described a new measure to classify differentially expressed genes and we compared it against the B-rank statistic as a standard method. According to this new classification method, the biological functions overrepresented in top differentially expressed genes when comparing tumor versus control samples were associated with growth, differentiation, immune system response, communication, cellular matrix and enzyme regulation. Comparing superficial versus invasive samples, the most important overrepresented biological category was growth and, specifically, DNA synthesis and mitotic cytoskeleton. On the other hand, some under expressed genes have been clearly related to muscular tissue contamination in control samples. Finally, we demonstrated that a pool strategy could be a good option to detect the best differentially expressed genes between two compared conditions. Experiment Overall Design: We analyzed gene expression profiles in normal bladder tissues (controls), low grade superficial tumor samples (pathologically classified as Ta low grade, named as Ta), high grade superficial tumors with an unclear clinical behavior (T1 high grade, named as T1) and high grade muscle invasive tumors (pathologically classified as T2, T3 or T4, named as T2+). We analyzed data using a sub-pooling strategy. The number of individual samples on every pool was: controls (4, 4, 4), Ta (5, 5, 5), T1 (5, 4, 4) and T2+ (5, 5, 5).
2008-06-15 | E-GEOD-7476 | biostudies-arrayexpress
Project description:Activation of oncogenic ras pathway accounts for up to 90% low-grade superficial urothelial carcinomas of bladder, and p53 deficiency is very common in high-grade muscle invasive carcinomas. These two pathways in bladder urothelial tumorigenesis used to be considered divergent and their potential collaboration has not been illustrated. We did laser capture micro-dissection (LCM) to separate the tumor cells from the whole bladder tissues from H-ras transgenic and p53 knockout mice, as well as normal urothelial cells as control. Microarray was then performed to identify distinct classes of up-regulated genes during tumorigenesis and progression. In order to get the gene expression profiles of carcinoma in situ (CIS), muscle invasive tumors and normal cells, we used LCM to purify the cells from mixture of different types of cells, and then extracted RNA for microarray. There are three groups applied in microarray, which are normal cells as control, CIS (tumor genesis) and invasive tumors (tumor progression).
2015-01-08 | E-GEOD-64756 | biostudies-arrayexpress
Project description:Identification of bladder cancer subsets
2014-02-10 | GSE48075 | GEO
Project description:Background: Although histology is the corner stone for decision analysis in bladder cancer, it still needs refinement and new tools to better identify tumours with the highest risk of progression or recurrence. Objective: We designed a prospective study to evaluate whether microarray analysis could find a molecular signature for pathologic staging and/or grading. Design, setting and participants: Prospective multicentric study conducted from September 2007 to May 2008 (108 bladder tumours (45 pTa, 35 pT1 and 28> pT1)). Microarray analysis was performed with Agilent Technologies Human Whole Genome 4 x 44K oligonucleotide microarrays and used a method of dual color type versus a reference consists of a pool of tumours. From the lists of genes provided by the BrB Class Comparison analyses, we validated the microarray results of 38 selected differentially expressed genes by RT-QPCR in another bladder tumour cohort (n = 95). Results: The cluster M-^Ssuperficial vs invasive stageM-^T properly classified 92.9% of invasive stages and 66.3% of superficial stages. Among the superficial tumours, the cluster analysis showed that pT1b tumours were closer to invasive stages than pT1a tumours. We also found molecular differences between low and high-grade superficial tumours. However these differences were less caricatural than the one observed for staging.Conclusions: We confirm that the histopathological classification into subgroups pTa, pT1a and pT1b may have a translation in a M-^Smolecular signatureM-^T with a continuous progression of deregulation (overexpression or repression of these genes) from superficial (pTa) to more invasive (pT1a then b stage).
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Project description:We profiled two repressive histone modifications (H3K9m3 and H3K27m3) using ChIP-Seq in normal urothelial cells and cell lines representing non-invasive and invasive tumors. Two bladder cancer cell lines (RT112 and EJ/T24 from ATCC) and normal human urothelial (NHU) cells were treated according to standard ChIP-Seq protocols using antibodies against the histone modifications H3K9m3 and H3K27m3 (from Millipore). The sequencing reads were mapped against the human genome (GRCh37/hg19).
2011-08-03 | E-GEOD-31125 | biostudies-arrayexpress
Project description:Expression profile of non-muscle invasive (superficial) bladder carcinoma
2015-07-27 | E-MTAB-1940 | ExpressionAtlas