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Urine of bladder cancer and controls

ABSTRACT: urine of bladder cancer and controls Raw sequence reads

PROVIDER: PRJNA486651 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8114930.fastq.gz	Fastqsanger.gz
	SRR8114940_1.fastq.gz	Fastqsanger.gz
	SRR8114940_2.fastq.gz	Fastqsanger.gz
	SRR8114950.fastq.gz	Fastqsanger.gz
	SRR8114950_1.fastq.gz	Fastqsanger.gz

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Project description:Objective was to identify urine cell-free microRNAs enabling early non-invasive detection of bladder cancer. Total RNA enriched for fraction of short RNAs was isolated using Urine microRNA purification kit (Norgen corp.). miRNA profiles were determined using the Affymetrix GeneChip miRNA 3.0 array and analyzed to identify differentially deregulated miRNA in bladder cancer patients compared with helathy controls.

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Identification of a novel set of DNA methylation markers in bladder cancer using MBD-methylCap/seq and urine DNA screening in a Chinese population

Project description:The aim of the present study was to identify novel DNA methylation markers in bladder cancer (BCa) through genome-wide profiling of bladder cancer cell lines and subsequent MSP screening in urine samples. Experimental Design: MBD methylCap/seq was carried out to screen differentially methylated CpG islands using two BCa cell lines (5637 and T24) and two normal bladder mucosa (BM) samples. The top one hundred most hypermethylated targets were screened using Methylation Specific PCR (MSP) in small and big cohort of urine samples from BCa patients and normal controls. The diagnostic performance of the gene panel was further evaluated in different clinical scenarios. Results: In total, 1,627 gene promoter regions hypermethylated in BCa cell line were identified in genomic level methylation profiling. The followed screening procedure in clinical urine sample generated eight genes (VAX1, KCNV1, ECEL1, TMEM26, TAL1, PROX1, SLC6A20, and LMX1A) capable of differentiating BCa from normal control. Subsequent validation in a large sample size enabled the optimisation of 5 methylation targets (VAX1, KCNV1, TAL1, PPOX1 and CFTR) for BCa diagnosis with sensitivity and specificity of 86.32% and 87.13%, respectively. In addition, VAX1 and LMX1A methylation could predict the tumour recurrence. Conclusions: Tumor specific biomarkers of BCa could be established by first performing genome level methylation profiling with cell lines and then screening the potential targets in urine samples. The panel of methylated genes identified was promising for the early non-invasive detection and surveillance of BCa. MBD methylCap/seq was carried out to screen differentially methylated CpG islands using two BCa cell lines (5637 and T24), and two normal bladder tissue mix as control.

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Gene expression analysis of urine sediment: evaluation for potential noninvasive markers of interstitial cystitis/bladder pain syndrome

Project description:Purpose: Determine if gene expression profiles in urine sediment could provide non-invasive candidate markers for painful bladder syndrome (PBS) with and/or without Hunner lesions. Materials and Methods: Fresh catheterized urine was collected and centrifuged from control (n = 5), lesion-free (n = 5), and Hunner lesion bearing (n = 3) patients. RNA was extracted from the pelleted material and quantified by gene expression microarray (Affymetrix Human Gene ST Array). Results: Three biologically likely hypotheses were tested: A) all three groups are distinct from one another; B) controls are distinct from both types of PBS patients combined, and C) Hunner lesion PBS patients are distinct from controls and non-Hunner-lesion PBS combined. For statistical parity an unlikely fourth hypothesis was included: non-Hunner-lesion PBS patients are distinct from controls and Hunner lesion PBS combined. Analyses supported selective upregulation of genes in the Hunner lesion PBS group (hypothesis C), and these were primarily associated with inflammatory function. This profile is similar to that reported in a prior microarray study of bladder biopsies in Hunner lesion PBS. Conclusions: Urine sediment gene expression from non-Hunner-lesion PBS patients lacked a clear difference from that of control subjects, while the array signatures from PBS patients with Hunner lesions showed a clear, primarily inflammatory, signature. This signature was highly similar to that seen in a prior microarray study of bladder biopsies. Thus, although sample sizes were small, this work suggests that gene expression in urine sediment may provide a non-invasive biomarker for Hunner lesion, but not non-Hunner lesion, PBS.

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