Browse
Submit Data
Databases
API
Help

Dataset Information

16 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 5

Renal Follow Up Series

ABSTRACT: This study's purpose is to use data generated in Renal whole genome and exome Cancer sequencing to target specific areas in multiple other Renal Cancer samples. These areas will then be subjected to bespoke pull downs, tagged and then pool the resultant amplicons. These amplicons will then be sequenced. This is hoped to show the prevalence of previous findings in multiple individuals in a high throughput method.

PROVIDER: EGAS00001000095 | EGA |

REPOSITORIES: EGA

ACCESS DATA

Json Xml

Similar Datasets

Breast Cancer Follow Up Series

Project description:This study's purpose is to use data generated in whole genome and exome Breast Cancer sequencing to target specific areas in multiple other Breast Cancer samples. These areas will then be subjected to PCR in multiple cases, tagged and then pool the resultant amplicons. These amplicons will then be sequenced on the Illumina GAII. This is hoped to show the prevalence of previous findings in multiple individuals in a high throughput method.

| EGAS00001000002 | EGA

Myelodysplastic Syndrome Follow Up Series

Project description:Agilent whole exome hybridisation capture was performed on genomic DNA derived from MDS and matched normal DNA from the same patients. Next Generation sequencing performed on the resulting exome libraries and mapped to build 37 of the human reference genome to facilitate the identification of novel cancer genes. Now we aim to discover the prevalence of our findings using bespoke pulldown methods and sequencing the products from a larger set of patient DNA.

| EGAS00001000224 | EGA

Sarcoidosis + Follow-up study

Project description:Sarcoidosis + Follow-up 6 month after Keywords = sarcoidosis Keywords = follow-up Keywords: other

2005-01-18 | GSE1907 | GEO

Follow-up-IBS

Project description:Follow-up of faecal microbiota in IBS patients

| PRJEB3227 | ENA

Myeloma Follow up Pilot

Project description:Targeted capture of exonic and intronic regions of interest for the study of genomic alterations in multiple myeloma.

| EGAS00001000743 | EGA

Indonesian schoolchildren - follow-up

Project description:Bacterial gut microbiota composition of Indonesian schoolchildren from urban Makassar - follow-up

| PRJEB40889 | ENA

CD follow-up study

Project description:The stability of the fecal microbiota in Crohn’s disease patients with changing disease course

| PRJEB20076 | ENA

Bull seminal plasma proteomes follow-up

Project description:Analysis of seminal plasma from 17 bulls used for inseminations

2021-06-14 | PXD021245 | Pride

mRNA-seq data for KMT2D HNSCC (follow-up)

Project description:Head and neck squamous cell carcinoma (HNSCC) is the sixth most common cancer worldwide, with 5-year survival of ~50%. Genomic profiling studies have identified important somatic mutations in this disease which presents an opportunity for precision medicine. We demonstrate that KMT2D, a histone methyltransferase harbors somatic mutations in ~17% of HNSCC and is associated with 2-year recurrence in TCGA data. Consistent with algorithmic prediction of bring a driver tumor-suppressor event, its loss results in larger oral tumors in immune-proficient orthotopic models. Mechanistically, we find that KMT2D knockdown or KMT2D mutation causes loss of H3K4me1-marked enhancers harboring IRF7/9 binding sites, which is known to regulate interferon signaling. Indeed, KMT2D loss in human and murine cell lines deregulated transcriptional levels of cytokine expression and impacted numerous immune signaling pathways, including interferon signaling. Consistently, Kmt2d knockdown in murine tumors exhibited decrease in IFN-producing effector T cells and an increase in T-cells with an exhausted phenotype. Epistasis experiments showed that exogenous treatment with IFNabrogated the increased tumor growth in Kmt2d-deficient oral tumors. Together, these results support the role of KMT2D as a tumor suppressor in HNSCC that regulates the tumor microenvironment by modulating H3K4me1-marked enhancers controlling interferon signaling.

2022-10-06 | GSE185536 | GEO