Kinome expression profiling of muscle invasive bladder cancer (MIBC) patients
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ABSTRACT:
PROVIDER: PRJNA541420 | ENA |
REPOSITORIES: ENA
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Project description:Muscle invasive bladder cancer (MIBC) is one of the aggressive cancer with limited treatment options. Targeted gene expression profiling in normal and tumor samples from MIBC patients could aid in identification of potential therapeutic targets. Thus we used kinase specific panel to study their expression pattern and to identify targetable genes.
2020-04-20 | GSE130598 | GEO
Project description:Background: Bladder-sparing trimodality therapy (TMT) is an alternative to radical cystectomy (RC) for muscle-invasive bladder cancer (MIBC), and biomarkers to inform therapy selection are needed. Objective: To evaluate immune and stromal signatures in MIBC treated with TMT.
2019-03-23 | GSE128701 | GEO
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: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: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:Muscle-invasive bladder cancer (MIBC) is an aggressive disease with high morbidity and mortality that can be divided into basal and luminal subtypes based on genomic characteristics. Due to the complex heterogeneity of MIBC, specific markers are needed to distinguish MIBC subtypes to guide future clinical treatment. In this study, we explore abnormal lncrnas that are specific to the basic and intracavitary subtypes of MIBC, which will provide potential biomarkers for precision therapy of MIBC.
2023-04-14 | GSE229410 | GEO
Project description:The goals of this study are to screen differential expression profiles of tRNA-Derived small RNAs (tsRNAs) in muscle-invasive bladder cancer (MIBC) in Chinese population using next-generation sequencing and qRT-PCR.As a result, in MIBC tissues, 406 tsRNAs were differentially expressed between in MIBC tissues. Of them, 91 tsRNAs were significantly differentially expressed (fold change>1.5; P<0.05): 65 tsRNAs were significantly up-regulated whereas 26 were significantly down-regulated in MIBC.Taken together,this study explored, for the first time, the significant alteration of tsRNA expression profiles in MIBC in Chinese population and offered deep insights into many possible treatment targets of MIBC by regulating tsRNAs.
2022-04-27 | GSE192651 | GEO
Project description:Muscle invasive bladder cancer (MIBC) is highly heterogeneous, both at the molecular level and in terms of clinical progression. Several molecular classifications have been proposed to understand this heterogeneity and contribute to diagnosis and treatment. Although the neuroendocrine-like subtype is the most aggressive and exhibits the worst survival rate when compared to other subtypes, molecular mechanisms underlying neuroendocrine differentiation have not yet been understood. The nuclear localization of β-catenin is known to be associated with the activation of the Wnt/β-catenin pathway, and it is linked to disease progression and aggressiveness in various cancer types. To decipher the mechanisms underlying the neuroendocrine differentiation of bladder cancer, we determined β-catenin expression profiles of 169 T2-stage primary MIBC samples. Immunohistochemistry analysis revealed increased expression of the most widely used NE markers SYP, CGA, and CD56 in β-catenin positive MIBC tumors. As a result of our transcriptomic analysis, we observed higher expression of neuroendocrine differentiation-related genes, and lower expression of basal differentiation and urothelial differentiation-related genes in β-catenin positive MIBC tumors. Furthermore, we applied a molecular consensus classifier to β-catenin positive and negative samples, and the NE score was significantly higher in β-catenin positive MIBC compared to others. By comparing transcriptome profiles, we reveal that β-catenin positive MIBC harbor unique gene modules and gene expression profiles that are divergent from the β-catenin negative MIBC. GO term and KEGG pathway analyses showed that various neurogenesis-related pathways as well as regulation of gene expression and chromatin remodeling were significantly enriched at β-catenin positive MIBC. Our results collectively revealed that β-catenin expression contributes to neuroendocrine differentiation of bladder cancer.
2024-07-16 | GSE253064 | GEO
Project description:High mortality rate of muscle-invasive bladder cancer (MIBC) and complexity of disease demand new multi-targeting treatment strategies. Targeting proliferating cell nuclear antigen (PCNA) with a peptide containing the AlkB homologue 2 PCNA interacting motif (APIM), is shown to impair multiple vital cellular stress responses and induce hypersensitivity against several chemotherapeutics in different pre-clinical models. This study examine the anti-cancer efficacy of the novel APIM-peptide drug when combined with cisplatin-based therapies (cisplatin, cisplatin/gemcitabine (GC) and methotrexate/vinblastine/adriamycin/cisplatin (MVAC)) in a panel of bladder cancer (BC) cells and with intravenous cisplatin-therapy in a rat MIBC-model. Furthermore, we explore the molecular mechanisms underlying the observed effects on a genomic, proteomic and metabolomic level using microarray, multiplexed inhibitor bead (MIB)-assay, and targeted mass spectrometric metabolite profiling. The APIM-peptide significantly increased the efficacy of all cisplatin-based therapies in all BC cell lines tested, including a cisplatin resistant cell line and reduced the tumor load in cisplatin treated MIBC-bearing rats. Genome and proteome analysis of APIM-peptide/cisplatin treated BC cells revealed reduced expression of multiple proteins frequently overexpressed in MIBC. Of notice, the EGFR/ERBB2, PI3K/Akt and MAPK signaling pathways and anti-apoptosis were downregulated. We suggest that the anti-cancer effect of the APIM-peptide is through the downregulation of several known oncogenic signaling pathways including anti-apoptosis. Together our results indicate that the APIM-peptide represents a potential improved treatment approach for patients with MIBC.
2018-09-10 | PXD008724 | Pride
Project description:Four different molecular classifications of muscle-invasive bladder cancer (MIBC) based on gene expression have been proposed. With the ultimate goal of utilizing these molecular subtypes for personalized treatment, we investigated their significance in the context of neoadjuvant cisplatin-based chemotherapy (NAC).
2017-05-25 | GSE87304 | GEO