Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Homo sapiens

ABSTRACT: Mismatch repair proteins expression and tumor-infiltrating T-cells in colorectal cancer

PROVIDER: PRJDB13754 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	DRR381291.fastq.gz	Fastqsanger.gz
	DRR381292.fastq.gz	Fastqsanger.gz
	DRR381293.fastq.gz	Fastqsanger.gz
	DRR381294.fastq.gz	Fastqsanger.gz
	DRR381295.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Homo sapiens

Project description:Deciphering the Paradox: Microsatellite Instability Amid Mismatch Repair Proficiency in Colorectal Cancer

| PRJNA1052979 | ENA

A Single Cell Atlas of MMRd and MMRp Colorectal Cancer

Project description:Immune responses to cancer are highly variable, in particular colorectal cancer tumors with mismatch repair-deficiency (MMRd) show an elevated presence and activity of immune cells as compared to mismatch repair proficient tumors. To understand the immune response patterns, and key differences between these types of colorectal cancer, we transcriptionally profiled 371,223 tumor and adjacent normal cells from 28 MMRp and 34 MMRd patients. Unsupervised analysis identified 88 cell subsets, from 7 distinct cell lineages, and an associated compendium of 204 gene expression programs. Examination of these programs revealed extensive transcriptional and spatial reprogramming, characteristic to MMRd and MMRp tumors.

2021-08-26 | GSE178341 | GEO

Project description:colorectal cancer with mismatch Repair status

| PRJNA871771 | ENA

Gene expression profiling of colorectal cancers to understand molecular changes and clinicopathological features

2009-03-01 | GSE10982 | GEO

Gene expression profiling of colorectal cancers to understand molecular changes and clinicopathological features

Project description:Gene expression was analyzed in terms of canonical molecular changes and clinicopathological features to elucidate alternative or subordinate pathways during colorectal tumorigenesis and tumor growth. Eighty-four sporadic colorectal cancer patients, standardized by tumor location, were consecutively enrolled. Representative molecular changes including APC, TP53, Wnt, RAF, and mismatch repair defect (MMR) were recorded for each sample. Keywords: disease state analysis; sub-type analysis within colorectal cancers 84 samples from colorectal patients were analyzed. Paired tumor and adjacent normal tissues from the same patient were used for hybridization onto custom-made, 21k dual channel cDNA arrays. We prepared a similar number of samples from each of the three tumor locations (ascending 27, descending 29, and rectum 28) and recorded for each sample important molecular changes such as APC, TP53, RAF, WNT, and MMR mutations.

2009-02-28 | E-GEOD-10982 | biostudies-arrayexpress

Rhesus Macaque Model of Mismatch Repair-Deficient Colorectal Cancer

Project description:Rhesus Macaque Model of Mismatch Repair-Deficient Colorectal Cancer

| PRJNA738804 | ENA

Homo sapiens

Project description:Immunogenomic analysis of tumor infiltrating B cells in gastric cancer

| PRJDB10542 | ENA

Mismatch-repair signature mutations activate gene enhancers across human colorectal cancer epigenomes

Project description:We show that mismatch-repair (MMR) signature mutations can activate colorectal cancer (CRC)-specific enhancers, through analysis of enhancer DNA associated with the active enhancer histone mark H3K27ac. We demonstrate that MMR mutations activate enhancers using a xenograft metastasis model, where mutations are induced naturally via CRISPR/Cas9 inactivation of MLH1 prior to tumor cell injection.

2019-02-07 | GSE126188 | GEO

MBD4 loss results in global reactivation of promoters and retroelements with low methylated CpG density.

Project description:Inherited defects in the base-excision repair gene MBD4 predispose individuals to adenomatous polyposis and colorectal cancer, which is characterized by an accumulation of C>T transitions resulting from spontaneous deamination of 5’-methylcytosine. Despite its significance, this DNA repair pathway is still poorly understood. Here we show that the protein MBD4 is required for DNA methylation maintenance and G/T mismatch repair. Transcriptome and methylome analyses reveal a genome-wide hypomethylation of promoters, gene bodies and repetitive elements in the absence of MBD4 in vivo. Methylation mark loss is accompanied by a broad transcriptional derepression phenotype affecting promoters and retroelements with low methylated CpG density. MBD4 in vivo forms a complex with the mismatch repair proteins (MMR), which exhibits high bi-functional glycosylase/AP-lyase endonuclease specific activity towards methylated DNA substrates containing a G/T mismatch. Experiments using recombinant proteins reveal that the association of MBD4 with the MMR protein MLH1 is required for this activity. The described data identify MBD4 as an enzyme specifically designed to repair deaminated 5-methylcytosines and illustrates how MBD4 functions in normal and pathological conditions.

2022-01-10 | GSE84318 | GEO