Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1078523 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28022182_1.fastq.gz | Fastqsanger.gz | |||
| SRR28022182_2.fastq.gz | Fastqsanger.gz | |||
| SRR28022183_1.fastq.gz | Fastqsanger.gz | |||
| SRR28022183_2.fastq.gz | Fastqsanger.gz | |||
| SRR28022184_1.fastq.gz | Fastqsanger.gz |
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Project description:Differential neoadjuvant chemotherapy response in urothelial carcinoma molecular subtypes
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Project description:<p>Cisplatin-based chemotherapy is the standard of care for patients with muscle invasive urothelial carcinoma. Pathologic downstaging to pT0/pTis after neoadjuvant cisplatin-based chemotherapy is associated with improved survival, and some patients with metastatic disease achieve complete responses to these therapies. However, the molecular determinants of cisplatin response are incompletely understood. We performed whole exome sequencing on tumor and germline DNA from patients with muscle invasive or metastatic urothelial carcinoma who received cisplatin-based chemotherapy to identify somatic mutations that occurred preferentially in cisplatin responders.</p>
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Project description:Metastatic urothelial carcinoma (UC) of the bladder is associated with multiple somatic copy number alterations (SCNAs). We evaluated SCNAs to identify predictors of poor survival in patients with metastatic UC treated with platinum chemotherapy.
2013-07-07 | GSE39280 | GEO
Project description:Metastatic urothelial carcinoma (UC) of the bladder is associated with multiple somatic copy number alterations (SCNAs). We evaluated SCNAs to identify predictors of poor survival in patients with metastatic UC treated with platinum chemotherapy.
2013-07-07 | GSE39281 | 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. 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:For patients with muscle-invasive bladder cancer, there are no biomarkers in clinical use that can identify patients that are sensitive or resistant to neoadjuvant chemotherapy. This study investigates how molecular subtypes impact pathological response and survival in 149 patients receiving preoperative cis-platin based chemotherapy by tumor classification using transcriptomic profiling and a 13-marker immunostaining panel. Furthermore, we explored to what extent gene expression signatures can predict chemotherapy response beyond molecular subtypes. We observed improved pathological response rates and survival outcomes for patients presenting with genomically unstable (GU) and urothelial-like (Uro) subtypes compared to the basal-squamous (BASQ) subtype following neoadjuvant chemotherapy and radical cystectomy. Also, SPP1, coding for osteopontin, displayed a clear subtype-dependent effect on chemotherapy response, confirmed at the protein level. Based on our findings, we hypothesize that urothelial cancer of the luminal-like GU- and Uro-subtypes are more responsive to cisplatin-based chemotherapy which may influence patient selection pending further research.
2021-11-19 | GSE169455 | 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:Urothelial carcinoma of the bladder, the second most prevalent cancer within the urothelial system, often evades immune recognition by natural killer (NK) cells, but studies have shown that cyproheptadine (CPH), an anti-histamine drug, exhibits anticancer effects in this carcinoma. Co-culturing CPH-treated cells with NKG2D-expressing NK92 cells resulted in enhanced NK-mediated lysis of UC cells, with RNA-seq analysis revealing increased expression of the NKG2D ligand ULBP2 in CPH-treated cells. We hypothesize that cyproheptadine as a epigenetic modifier enhances NK-mediated cytotoxicity by restoring NKG2D ligands and CCL3 and as a control we used entinostat a known FDA approved HDAC1/3 inhibitor. Targeting NK cells offers a promising strategy against urothelial carcinoma. Further analysis showed epigenetic regulation of ULBP2 expression with increased H3K27Ac active mark enrichment in CPH-treated cells. Overexpression of ULBP2 led to increased NK-mediated lysis, while knockdown reduced it in CPH-treated urothelial carcinoma cells. Additionally, CPH treatment enhanced the anti-tumor effect in a mouse model, likely due to increased NK and NKT cell infiltration. In summary, CPH triggers an innate immune response against urothelial carcinoma by promoting NK cell-mediated cytotoxicity through ULBP2 and CCL3 restoration.
2025-06-24 | GSE266660 | GEO
Project description:In bladder, loss of mammalian Sonic Hedgehog (Shh) accompanies progression to invasive urothelial carcinoma, but the molecular mechanisms underlying this cancer-initiating event are poorly defined. Here, we show that loss of Shh results from hypermethylation of the CpG shore of the Shh gene, and that inhibition of DNA methylation increases Shh expression to halt the initiation of murine urothelial carcinoma at the early stage of progression. In full-fledged tumors, pharmacologic augmentation of Hedgehog (Hh) pathway activity impedes tumor growth, and this cancer-restraining effect of Hh signaling is mediated by the stromal response to Shh signals, which stimulates subtype conversion of basal to luminal-like urothelial carcinoma. Our findings thus provide a basis to develop subtype-specific strategies for the management of human bladder cancer.
2019-04-09 | GSE129441 | GEO
Project description:The Phase 3 1L urothelial carcinoma (IMvigor130) trial revealed more favorable effects on overall survival with atezolizumab combined with gemcitabine and cisplatin (GemCis) than with atezolizumab combined with gemcitabine and carboplatin (GemCarbo). This study investigates the immunomodulatory effects of cisplatin vs carboplatin as a potential explanation for these clinical observations. GemCis compared with GemCarbo ± atezolizumab induced transcriptional changes in circulating immune cells, including upregulation of antigen presentation and T-cell activation programs. In vitro experiments demonstrated that cisplatin, compared with carboplatin, exerted direct immunomodulatory effects on cancer cells, promoting dendritic cell activation and antigen-specific T cell killing. These results underscore the key role of immune modulation in cisplatin's efficacy in urothelial carcinoma and highlight the potential importance of specific chemotherapy backbones for immune checkpoint blockade combination therapies.
2023-11-02 | GSE235066 | GEO