554b3a8c-0eb7-440b-b001-0f38c671bd4b - samples
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ABSTRACT:
PROVIDER: EGAD00001007005 | EGA |
REPOSITORIES: EGA
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Project description:miRNAs are involved in cancer development and progression,acting as tumor suppressors or oncogenes. Half of the human miRNAs are located in cancer-associated genomic regions and can function as tumor suppressor genes or oncogenes depending on their targets miRNA profiling was performed on paired bladder cancer tissues and differentially expressed miRNAs were identified in BC and adjacent noncancerous tissues of any disease stage/grade. Ten paired bladder cancer tissues (5 low-grade non-muscle-invasive bladder cancer[NMIBC] and 5 high-grade muscle-invasive bladder cancer[MIBC]) were sent to CapitalBio Corp. (Beijing) for noncoding RNA microarray analysis. The microarray analysis was done as described on the Web site of CapitalBio. NMIBC samples include 07A, 19A, 23A, 24A and T63 while coresponding pairs include 07B, 19B, 23B, 24B and 63. MIBC samples include 10A, 20A, 21A, 34A and 49A while coresponding pairs include 10B, 20B, 21B, 34B and 49B.
2012-07-06 | E-GEOD-39093 | biostudies-arrayexpress
Project description:Bladder cancer, one of the most prevalent malignancies worldwide, remains hard to classify due to a staggering molecular complexity. Despite a plethora of diagnostic tools and therapies, it is hard to outline the key steps leading up to the transition from high-risk non–muscle-invasive bladder cancer (NMIBC) to muscle-invasive bladder cancer (MIBC). Carcinogen-induced murine models can recapitulate urothelial carcinogenesis and natural anti-tumor immunity. Herein, we have developed and profiled a novel model of progressive NMIBC based on 10 weeks of OH-BBN exposure in hepatocyte growth factor/cyclin dependent kinase 4 (R24C) (Hgf-Cdk4R24C) mice. The profiling of the model was performed by histology grading, single cell transcriptomic and proteomic analysis, while the derivation of a tumorigenic cell line was validated and used to assess in vivo anti-tumor effects in response to immunotherapy. Established NMIBC was present in females at 10 weeks post OH-BBN exposure while neoplasia was not as advanced in male mice, however all mice progressed to MIBC. Single cell RNA sequencing analysis revealed an intratumoral heterogeneity also described in the human disease trajectory. Moreover, although immune activation biomarkers were elevated in urine during carcinogen exposure, anti-programmed cell death protein 1 (anti-PD1) monotherapy did not prevent tumor progression. Furthermore, anti-PD1 immunotherapy did not control the growth of subcutaneous tumors formed by the newly derived urothelial cancer cell line. However, treatment with CpG-oligodeoxynucleotides (ODN) significantly decreased tumor volume, but only in females. In conclusion, the molecular map of this novel preclinical model of bladder cancer provides an opportunity to further investigate pharmacological therapies ahead with regards to both targeted drugs and immunotherapies to improve the strategies of how we should tackle the heterogeneous tumor microenvironment in urothelial bladder cancer to improve responses rates in the clinic.
2021-06-09 | GSE174182 | GEO
Project description:Clinical management of bladder carcinomas (BC) remains a major challenge and demands comprehensive multi-omics analysis for better stratification of the disease. Identification of patients on risk requires identification of signatures predicting prognosis risk of the patients. Understanding the molecular alterations associated with the disease onset and progression could improve the routinely used diagnostic and therapy procedures. In this study, we investigated the aberrant changes in N-glycosylation pattern of proteins associated with tumorigenesis as well as disease progression in bladder cancer. We integrated and compared global N-glycoproteomic and proteomic profile of urine samples from bladder cancer patients at different clinicopathological stages (non-muscle invasive and muscle-invasive patients (n=5 and 4 in each cohort)) with healthy subjects (n=5) using SPEG method. We identified 635 N-glycopeptides corresponding to 381 proteins and 543 N-glycopeptides corresponding to 326 proteins in NMIBC and MIBC patients respectively. Moreover, we identified altered glycosylation in 41 NMIBC and 21 MIBC proteins without any significant change in protein abundance levels. In concordance with the previously published bladder cancer cell line N-glycoproteomic data, we also observed dysregulated glycosylation in ECM related proteins. Further, we identified distinct N-glycosylation pattern of CD44, MGAM and GINM1 between NMIBC and MIBC patients, which may be associated with disease progression in bladder cancer. These aberrant protein glycosylation events would provide a novel approach for bladder carcinoma diagnosis and further define novel mechanisms of tumor initiation and progression.
2020-09-10 | PXD020078 | Pride
Project description:This RNA-sequencing cohort includes 52 Non-muscle Invasive Bladder cancer (NMIBC) samples and 6 Muscle Invasive Bladder cancer (MIBC) samples.
| EGAS00001004358 | EGA
Project description:Because cystoscopy is expensive and invasive, a new method of detecting non-invasive muscular bladder cancer (NMIBC) is needed. This study aims to identify potential serum protein markers for NMIBC to improve diagnosis and to found treatment approaches to avoid disease progression to a life-threatening phenotype (muscle-invasive bladder cancer, MIBC). Here, silver nanoparticles (AgNPs, 9.73 ± 1.70 nm) as a scavenging device together with Sequential Window Acquisition of All Theoretical Mass Spectra (SWATH-MS) were used to quantitative analyze the blood serum protein al-terations in two NMIBC subtypes: T1 and Ta, and they were compared to normal samples (HC). NMIBC's analysis of serum samples identified three major groups of proteins, the relative content of which is different from the HC content: proteins implicated in the complement and coagulation cascade pathways and apolipoproteins. In conclusion, many biomarker proteins were identified that merit further examination to validate their useful significance and utility within the clinical management of NMIBC patients.
2022-02-15 | PXD028310 | Pride
Project description:Previous studies successfully revealed molecular characteristics of bladder cancers, dealing with non-muscle invasive bladder cancer and muscle invasive bladder cancer, separately. At the molecular level, however, there is a great need to aggregate these subtypes, which may share biological characteristics. This study aimed to identify distinct molecular subtypes of BC and the clinical and/or biological characteristics of each subtype. We used seven gene expression data sets for bladder cancer, which included data from 118 primary bladder cancer samples and 27 recurrent bladder tumor tissues from the Yonsei University Severance Hospital. Hierarchical clustering revealed four molecular subtypes of BC with different clinical outcomes: class 1 with low-grade NMIBC and the best prognosis; class 2 characterized by active FGFR3 and inhibited immune response pathways; class 3 with high-grade NMIBC and the worst progression-free survival; and class 4 mainly comprised of MIBC along with EMT activation. By applying the classifier based on these characteristics, we stratified all BC samples into newly identified molecular subtypes. When comparing previously reported subtypes, our subtypes well agreed with their molecular characteristics regardless of breast cancer-based biology, and showed a strong prognostic relevance in class 3. Integrative analysis of mutation and gene expression suggested that class 3 may have the potential benefit from anti-PD-L1 immunotherapy. Our classifier, constructed by NMIBC and MIBC integration, successfully stratified BC patients into distinct subtypes with different clinical outcomes and a possible treatment option.
2018-10-03 | GSE120736 | GEO
Project description:Bladder cancer is mostly present in the form of urothelium carcinoma, causing over 150.000 deaths each year. Its histopathological classification as muscle invasive and non-muscle invasive is the most prominent aspect, affecting the prognosis and progression of this disease. In this study, we defined the active regulatory landscape of MIBC and NMIBC cell lines using H3K27ac-seq and used an integrative data approach to combine our findings with existing data. Our analysis revealed FRA1 and FLI1 as the two critical transcription factors differentially regulating MIBC regulatory landscape. Importantly, we show that FRA1 and FLI1 regulate the genes involved in epithelial cell migration and cell junction organization. Knock-down of FRA1 and FLI1 in MIBC revealed the downregulation of several EMT-related genes such as MAP4K4 and FLOT1. Further, ChIP-SICAP performed for FRA1 and FLI1 enabled us to infer chromatin binding partners of these two transcription factors and link this information with their target genes, providing a comprehensive regulatory circuit for the genes implicated in invasive ability of the bladder cancer cells. Finally, we show that knock-down of FRA1 and FLI1 results in statistically significant less migration of cells using IC-CHIP assays. Our results collectively highlight the role of these two transcription factors in invasive characteristics of bladder cancer in selection and design of targeted options for treatment of MIBC.
2023-02-20 | GSE213533 | GEO
Project description:At diagnosis approximately 75% of bladder urothelial carcinomas are non muscle invasive bladder cancers (Ta, T1 and Tis), 20% are muscle invasive bladder cancer (T2-T4) and 5% are already metastatic. Non muscle invasive bladder cancers are characterized by tumor recurrence in 60% to 85% of cases and, therefore, long-term followup is needed. The current standard methods to detect and monitor bladder cancer are cystoscopy and cytology. Cystoscopy is an invasive method and cytology is hampered by low sensitivity, especially for low grade tumors. So there is need to develop reliable and noninvasive methods to detect and predict bladder cancer biological behavior. So we have performed high density oligonucleotide microarray for discovery of new molecular markers to diagnose and predict the outcome of bladder cancer.
2012-02-22 | GSE23732 | GEO
Project description:Tumor-blood paired whole-exome sequencing of 58 pairs of non-muscle-invasive bladder cancer samples (stageT1). Targeted sequencing of 112 non-muscle-invasive bladder cancer samples (34 stage T1; 78 stage Ta)
| EGAD00001008332 | EGA
Project description:Patients with high-risk non-muscle-invasive bladder carcinoma (NMIBC) frequently relapse after standard BCG immunotherapy and have a dismal outcome after progression to muscle-invasive bladder carcinoma (MIBC). Although BCG induces potent inflammatory responses upon intravesical instillations, the mechanisms of tumor resistance to such immunotherapy remain elusive. We performed a longitudinal immune profiling of a cohort of MIBC pre- and post BCG therapy with gene and protein expression analysis to establish correlations with 5 year clinical follow up. Here, we demonstrate two distinct patterns of BCG-induced immunosubversion, which include acquired immune resistance and tumor-cell intrinsic resistance. Firstly, intracellular BCG infection of a subset of urothelial carcinoma cells downregulated HLA-I expression and induced epithelial to mesenchymal transition (EMT) characteristics. BCG treated tumors exhibiting such HLA class I loss displayed an immune desert tumor microenvironment dominated by myeloid immunosuppressive cells. Such patients presented with early cancer relapses and a bad outcome. Conversely, BCG-treated tumors which did not lose HLA class I antigens at relapse displayed an immune escape mechanism dominated by a Th1 pattern with high expression of inhibitory checkpoints and exhaustion markers. Such patients had a favorable outcome upon second surgery. We surmise that HLA class I expression does not result from immunoediting but rather from an EMT process associated to myeloid immunosuppression that predicts dismal prognosis.
2022-05-05 | GSE199471 | GEO