Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

EGAS00001002988-sc-2019-04-11T08:44:36Z - samples

ABSTRACT: The aim of this project is to test whether HPV oncogenes and /or interferon induce the APOBEC mutational signature in vitro, and to test the role of APOBEC3A in this process. . This dataset contains all the data available for this study on 2019-04-11.

PROVIDER: EGAD00001004955 | EGA |

REPOSITORIES: EGA

ACCESS DATA

Json Xml

Similar Datasets

Role of HPV and Interferon in APOBEC mutational signature

Project description:The aim of this project is to test whether HPV oncogenes and /or interferon induce the APOBEC mutational signature in vitro, and to test the role of APOBEC3A in this process.

| EGAS00001002988 | EGA

EGAS00001002935-sc-2019-04-11T08:44:26Z - samples

Project description:We aim to describe the transcriptomic landscape of infant spindle cell tumours. . This dataset contains all the data available for this study on 2019-04-11.

| EGAD00001004954 | EGA

EGAS00001002929-sc-2019-04-11T08:44:19Z - samples

Project description:Single cell + bulk genomics study for immune and hematopoietic organs during human fetal development . This dataset contains all the data available for this study on 2019-04-11.

| EGAD00001004953 | EGA

Project description:2019 test data

| PRJNA827187 | ENA

Project description:2019 fungi test

| PRJNA827190 | ENA

Project description:2019 bacterial diversity test

| PRJNA827236 | ENA

Project description:2019 fungi diversity test

| PRJNA827242 | ENA

Proteomics of groundwater microbiomes collected from five wells in Alberta, Canada

Project description:Groundwater samples were collected from five wells in Alberta, Canada. The sampling location and time are indicated in the table below. 13 to 29 genomes were assembled from each metagenome. Proteomic analyses were performed to investigate which genomes and genes were expressed in each well. Sample ID Location Latitude (NAD 83) Longitude (NAD 83) Sampling date 19GWC19026 218 Cluny 50.85 -112.84 30/07/2019 19GWC19028 114 Ross Creek 49.99 -110.46 31/07/2019 19GWC19045 265 Metiskow 52.42 -110.61 18/09/2019 19GWE00050 991 Cynthia 56.22 -117.81 04/09/2019 19GWE00515 33 Fort McMurray 56.98 -111.85 17/09/2019

2024-05-21 | PXD044305 | Pride

Gene Expression Profiles of HPV-Positive and -Negative Head/Neck and Cervical Cancers

Project description:Human papillomaviruses (HPVs) are associated with nearly all cervical cancers (CCs), 20-30% of head and neck cancers (HNCs), and other cancers. Because HNCs also arise in HPV-negative patients, this type of cancer provides unique opportunities to define similarities and differences of HPV-positive versus HPV-negative cancers arising in the same tissue. Here, we describe genome-wide expression profiling of 84 HNCs, CCs and site-matched normal epithelial samples in which we used laser capture microdissection to enrich samples for tumor-derived versus normal epithelial cells. This analysis revealed that HPV+HNCs and CCs differed in their patterns of gene expression yet shared many changes compared to HPV-HNCs. Some of these shared changes were predicted, but many others were not. Notably, HPV+HNCs and CCs were found to be upregulated in their expression of a distinct and larger subset of cell cycle genes than observed in HPV-HNC. Moreover, HPV+ cancers over-expressed testis-specific genes that are normally expressed only in meiotic cells. Many, though not all, of the hallmark differences between HPV+HNC and HPV-HNC were a direct consequence of HPV and in particular the viral E6 and E7 oncogenes. This included a novel association of HPV oncogenes with testes specific gene expression. These findings in primary human tumors provide novel biomarkers for early detection of HPV+ and HPV- cancers, and emphasize the potential value of targeting E6 and E7 function, alone or combined with radiation and/or traditional chemotherapy, in the treatment of HPV+ cancers. Keywords: Gene expression ptofiles of primary cancers

2007-05-15 | GSE6791 | GEO

An APOBEC Cytidine Deaminase Mutagenesis in Human Cancers

Project description:Reprinted from Roberts et al. "An APOBEC cytidine deaminase mutagenesis pattern is widespread in human cancers", Nature Genetics, 45:970-976, 2013, with permission of Nature Publishing Group: Recent studies indicate that a subclass of APOBEC cytidine deaminases, which convert cytosine to uracil during RNA editing and retrovirus or retrotransposon restriction, may induce mutation clusters in human tumors. We show here that throughout cancer genomes APOBEC-mediated mutagenesis is pervasive and correlates with APOBEC mRNA levels. Mutation clusters in whole-genome and exome data sets conformed to the stringent criteria indicative of an APOBEC mutation pattern. Applying these criteria to 954,247 mutations in 2,680 exomes from 14 cancer types, mostly from The Cancer Genome Atlas (TCGA), showed a significant presence of the APOBEC mutation pattern in bladder, cervical, breast, head and neck, and lung cancers, reaching 68% of all mutations in some samples. Within breast cancer, the HER2-enriched subtype was clearly enriched for tumors with the APOBEC mutation pattern, suggesting that this type of mutagenesis is functionally linked with cancer development. The APOBEC mutation pattern also extended to cancer-associated genes, implying that ubiquitous APOBEC-mediated mutagenesis is carcinogenic.

| phs000677 | dbGaP

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data