Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression of Activation Induced Cytidine Deaminase and Risk of Transformation in Follicular Lymphoma

ABSTRACT: Expression of Activation Induced Cytidine Deaminase and Risk of Transformation in Follicular Lymphoma

PROVIDER: PRJNA815874 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Expression of Activation Induced Cytidine Deaminase and Risk of Transformation in Follicular Lymphoma

Project description:Expression of Activation Induced Cytidine Deaminase and Risk of Transformation in Follicular Lymphoma

| PRJNA815873 | ENA

A study of pharmacokinetic analysis of capecitabine and cytidine deaminase activity

Project description:Interventions: Blood samples(10 points) are collected after the first administration of capecitabine for pharmacokinetic analysis and cytidine deaminase activity measurement. Primary outcome(s): To evaluate the correlation AUC of 5-DFUR/AUC of 5-DFCR ratio and cytidine deaminase activity. Study Design: Single arm Non-randomized

| 2634538 | ecrin-mdr-crc

Base editing with a Cpf1–cytidine deaminase fusion

Project description:Base editing with a Cpf1–cytidine deaminase fusion

| PRJNA432936 | ENA

ChIP-seq Analysis of Activation-Induced Cytidine Deaminase Distribution in Human B Cells: Insights for Targeting Mechanisms

Project description:We report the analysis of genome wide distribution of activation induced cytidine deaminase by ChIP-seq in Human B cells. The resultant distribution of AID has then been compared to various histone modifications and transcription factors to shed insights into the mechanisms that target this enzyme.

2022-08-01 | GSE73933 | GEO

High-fidelity base editing mediated by Cpf1-cytidine deaminase fusion

Project description:High-fidelity base editing mediated by Cpf1-cytidine deaminase fusion

| PRJNA414402 | ENA

APOBEC Cytidine Deaminase Mutagenesis Pattern is Widespread in Human Cancers

Project description:APOBEC Cytidine Deaminase Mutagenesis Pattern is Widespread in Human Cancers

| PRJNA226256 | ENA

Role of activation-induced cytidine deaminase in the progression of follicular lymphoma.

Project description:Activation-induced cytidine deaminase (AID/AICDA) is required for somatic hypermutation and class-switch recombination of the immunoglobulin gene, and for c-myc translocation of germinal center-derived B-cell lymphoma. In the present study, we attempted to clarify the significance of AID associated with c-myc in the progression of follicular lymphoma (FL) using RT-PCR and quantitative real-time PCR. Tissues from the patients with grade 3 FL expressed relatively higher levels of c-myc and AID. The samples taken from a patient with FL who died within 2 years after the start of treatment showed either no or low expression of AID, despite expressing high levels of c-myc. In order to examine the role of AID expression in rapidly progressive FL, the full-length AID transcript was transfected into AID-negative cell lines established from different patients with rapidly progressive FL. This led to the establishment of AID-expressing transfectants with a low proliferation rate and a significantly increased incidence of G(0)/G(1) arrest compared with controls. Our results indicate that AID may act as a negative regulator of cell survival in FL when sufficient c-myc is expressed. Switch-off or low expression of AID after c-myc amplification may correlate with the clinical outcomes of FL.

| S-EPMC7713616 | biostudies-literature

New perspective on the origin of adaptive evolution: a study on cytidine deaminase in lampreys

Project description:This study evaluates the similarity of adaptive immune mechanisms between jawless and jawed vertebrates using lamprey cytidine deaminase (CDA). We identified the ancestral gene Lr-CDAs of the AID/APOBEC deaminase family and evaluated its biological function in vivo. Lr-CDA1 deletion affected the assembly of three types of variable lymphocyte receptors (VLRs). We identified a switch-like region in lamprey gVLRs bound to Lr-CDAs, which upon repression, downregulated VLRB expression. Overall, we propose that lampreys have an early form of class switch recombination (CSR) that is mediated by Lr-CDAs and acts on gVLRs, affecting the assembly, maturation, and diversity regulation of VLR genes in Lethenteron reissneri. This CSR process in lampreys is linked to tumorigenesis and chromosomal translocation markers via Lr-CDAs.

2024-04-16 | GSE252201 | GEO

Genome-wide copy number analyses reveal genomic abnormalities involved in transformation of follicular lymphoma

Project description:We studied 277 lymphoma samples (198 FL and 79 transformed FL [tFL]) using a single-nucleotide polymorphism array to identify the secondary chromosomal abnormalities that drive the development of FL and its transformation to diffuse large B-cell lymphoma. Affymetrix 250K NspI SNP arrays were performed according to the manufacturer's directions on DNA extracted from frozen follicular lymphoma or transformed follicular lymphoma tumor specimens

2015-03-30 | E-GEOD-67385 | biostudies-arrayexpress

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