Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Clonal evolution of platinum resistant urothelial carcinoma

ABSTRACT: Clonal evolution of platinum resistant urothelial carcinoma

PROVIDER: PRJNA315029 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Clonal Evolution of Platinum-Resistant Metastatic Urothelial Cancer

Project description:<p>Using whole-exome sequencing of urothelial carcinoma samples including matched sets of primary and locally recurrent or metastatic UC tumors collected over time and space and an in-depth analysis of tumors from two rapid autopsies, we provide the first detailed analysis of the therapy-driven clonal evolution of platinum-resistant urothelial carcinoma.</p> <p>We performed a systematic and integrated analyses for the molecular characterization of high-grade upper tract urothelial carcinomas (UTUC) using the whole-exome and mRNA sequencing. </p>

| phs001087 | dbGaP

Identification of the possible molecules by which acquired platinum resistance induces EMT-like changes in urothelial carcinoma

2016-07-01 | GSE58624 | GEO

Identification of the possible molecules by which acquired platinum resistance induces EMT-like changes in urothelial carcinoma

Project description:To identify the possible targets in EMT-acquisition after developing acquired platinum resistance in urothelial carcinoma (UC), we examined the changes in global gene expression before and after development of acquired platinum resistance. Comparing two types of acquired platinum resistant UC cells and their corresponding parent cells, in the end we identified 49 genes (25 up-regulated and 24 down-regulated genes) which were commonly changed in two acquired platinum resistant UC cells. Four invasive UC cell lines, T24, 5637, and those acquired platinum-resistant sublines T24PR and 5637PR, were used for microarrays. T24PR and 5637PR cells were newly established in our laboratory, which were grown and passaged upon reaching confluence in medium containing CDDP over a 6-month period. In preliminary studies, we found that these cell lines had an altered phenotype with morphologic and molecular changes consistent with EMT, and exhibited a marked difference in migratory potential before and after developing platinum resistance.

2016-07-01 | E-GEOD-58624 | biostudies-arrayexpress

Clonal evolution of chemotherapy-resistant urothelial carcinoma.

Project description: Not available

| S-EPMC5549141 | biostudies-literature

Molecular profiling of ovarian carcinoma platinum-sensitive and -resistant cell lines (microRNAs)

Project description:Resistance to platinum compounds represents a major obstacle to the cure of ovarian carcinoma. The molecular profiling of drug-sensitive and drug-resistant cells may be helpful to clarify if altered expression of miRNAs can contribute to the drug-resistant phenotype. The expression pattern of miRNAs of three ovarian carcinoma cell lines was examined. The analysis revealed the modulation of several miRNAs in the two platinum-resistant cell lines as compared to parental platinum-sensitive cells. The integration of the information obtained through miRNA expression analysis may be useful to clarify the specific molecular alterations of factors and pathway favouring survival of tumor cells.

2018-06-26 | GSE58469 | GEO

Molecular profiling of ovarian carcinoma platinum-sensitive and -resistant cell lines (gene expression)

Project description:Resistance to platinum compounds represents a major obstacle to the cure of ovarian carcinoma. The molecular profiling of drug-sensitive and drug-resistant cells may be helpful to clarify if altered gene expression can contribute to the drug-resistant phenotype. The expression pattern of three ovarian carcinoma cell lines was examined. The analysis revealed the modulation of several genes in the two platinum-resistant cell lines as compared to parental platinum-sensitive cells. The integration of the information obtained through gene expression analysis may be useful to clarify the specific molecular alterations of factors and pathway favouring survival of tumor cells.

2018-06-26 | GSE58470 | GEO

Transcriptome analysis for KDM6A mutated urothelial bladder carcinoma and EZH2 inhibitor treated KDM6A mutated urothelial bladder carcinoma

Project description:Purpose: The goals of this study are to compare 1. The transcription profile in KDM6A wildtype and KDM6A mutated urothelial bladder carcinoma. 2. The transcriptional changes in KDM6A mutated urothelial bladder carcinoma upon EZH2 inhibitor treatment.

2017-03-01 | GSE92723 | GEO

Homo sapiens

Project description:Clonal evolution of platinum resistant urothelial carcinoma

| PRJNA315030 | ENA

In-depth protein profiling of cytology samples in urothelial carcinoma

Project description:Urine cytologic examination is a widely used primary pathologic screening test in the diagnosis of bladder urothelial carcinoma (BLCA), however the low diagnostic accuracy remains challenging. We conducted high-throughput proteome on ten pairs of BLCA and benign urothelial lesion (BUL) to identify a supportive proteomic marker as an ancillary test in liquid based cytology (LBC).

2018-07-04 | PXD006805 | Pride

Intra-tumor heterogeneity and clonal evolution patterns towards platinum-resistant high-grade serous ovarian cancer

Project description:Although many high-grade serous ovarian carcinoma (HGSOC) patients are initially sensitive to the standard-of-care platinum-based therapy, intra-tumor heterogeneity may fuel selection towards platinum-resistant clones over subsequent lines of therapy. We performed whole-exome coupled to ultra-deep re-sequencing and copy number alteration (CNA) profiling on 31 matched diagnosis and relapse tumors from HGSOC patients treated with platinum. Genetic heterogeneity within tumor pairs varied extremely, with some recurrent tumors being identical and others completely different from the primary tumor. All primary tumors showed evidence of homologous recombination (HR)-deficiency, but none of them carried reactivating mutations in the HR pathway at relapse, also not when becoming resistant to subsequent lines of platinum. We did also not identify other mutations, CNAs or pathways that were enriched in platinum-resistant clones. However, a platinum score consisting of 13 CNAs correlated significantly with platinum-free interval (PFI) after first-line therapy in multiple cohorts of >450 primary HGSOCs. A relative increase of this score in the relapsed tumor correlated with a change in PFI during subsequent therapy. Clonal evolution under platinum therapy contributes to genetic heterogeneity within tumor pairs, implicating that genetic tests linked to targeted treatment options for recurrent HGSOC need to be performed on biopsies collected at relapse. Platinum resistance of an initially platinum-sensitive HR-deficient HGSOC at relapse is not caused by reactivation of the HR pathway, suggesting that these tumors are still responsive to PARP inhibitors, instead, several chromosomal aberrations contribute to a score predictive of disease outcome under platinum therapy, both in first and subsequent lines of platinum therapy.

| EGAS00001001244 | EGA

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data