Identification of Differential Tumor Subtypes of T1 Bladder Cancer
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA645686 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12202400.fastq.gz | Fastqsanger.gz | |||
| SRR12202401.fastq.gz | Fastqsanger.gz | |||
| SRR12202402.fastq.gz | Fastqsanger.gz | |||
| SRR12202403.fastq.gz | Fastqsanger.gz | |||
| SRR12202404.fastq.gz | Fastqsanger.gz |
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Project description:Stage T1 bladder cancers have the highest progression and recurrence rates of all non-muscle invasive bladder tumors. T1 tumors are heterogeneous; while most T1 patients are treated with BCG, many will progress and die from bladder cancer, and particularly aggressive tumors could be treated by early cystectomy. To better understand the molecular heterogeneity of T1 cancers, we performed transcriptome profiling and unsupervised clustering, identifying five consensus subtypes of T1 tumors treated with reTUR, induction and maintenance BCG. The T1-LumGU subtype was associated with CIS (6/13, 46% of all CIS), had high E2F1 and EZH2 expression, and enriched E2F target and G2M checkpoint Hallmarks. T1-Inflam was inflamed and infiltrated with immune cells. While most T1 tumors were classified as luminal papillary, the T1-TLum subtype had the highest median Luminal Papillary score and FGFR3 expression, no recurrence events, and the fewest copy number gains. T1-Myc and T1-Early subtypes had the most recurrences (14/30 within 24 months), highest median MYC expression, and, when combined, had significantly worse recurrence-free survival than the other three subtypes. T1-Early had 5 (38%) recurrences within the first 6 months of BCG, and repressed IFN-alpha and IFN-gamma Hallmarks and inflammation. We developed a single-patient T1 classifier and validated our subtype biology in a second cohort of T1 tumors. Future research will be necessary to validate the proposed T1 subtypes and to determine if therapies can be individualized for each subtype.
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Project description:Grainyhead-like transcription factor 3 (GRHL3) is known to affect cancer development depending on subtypes in various entities. Here, we analyzed the subtype-specific role of GRHL3 in bladder carcinogenesis comparing common urothelial carcinoma (UC) with squamous bladder cancers (sq-BLCA). We examined GRHL3 mRNA and protein expression in cohorts of patient samples, its prognostic role as well as its functional impact on tumorigeneses in different molecular and histopathological subtypes of bladder cancer. We showed for GRHL3 a reverse expression in squamous and urothelial bladder cancer subtypes. Stably GRHL3 overexpressing EJ28 and SCaBER in vitro models revealed a tumor suppressive function in squamous and a oncogenic role in the urothelial cancer cells affecting cell migratory and invasive capacities. Transcriptomic profiling demonstrated highly subtype specific GRHL3 regulated expression networks coined by enrichment of genes involved in integrin mediated pathways. In SCaBER loss of RhoA GTPase activity was demonstrated associated with co-regulation of EIF4E3, a potential tumor suppressor gene. Thus, our data provide for the first time a detailed insight into the role of the transcription factor GRHL3 in different histopathological subtypes of bladder cancer.
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Project description:Transcriptomic Analysis Of Micropapillary High Grade T1 Urothelial Bladder Cancer
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Project description:Management of high-grade T1 (HGT1) micropapillary bladder cancer (MPBC) is controversial. An accurate genomic characterization might help predict outcome. We analyze the transcriptomic profile of MPBC in a clinically annotated HGT1 cohort establishing correlation with clinical outcome.A retrospective analysis of prospectively clinically followed series of HGT1; 23 patients with MPBC and 64 without MPBC (reference set). We identified a set of genes differentially expressed (DE). Associations between; clinical variables and gene expression (GE) levels (Wilcoxon’s rank sum); GE and time to progression (TTP) in univariate analysis (Log rank); GE levels adjusting for clinical variables (Cox regression) were evaluated.We identified a 26-gene signature that characterized MPBC in HGT1. Several genes including CD36, FAPB3 and RAETE1 were significantly associated with TTP. High expression of FABP3 and CD36 were associated with shorter TTP (P=0.045 and P=0.08 (NS)) as was low expression of RAET1E (P=0.01). Limitations include the lack of specific quantification of the percentage of MPBC tumor >10%.
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