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Project #10906
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#10906 : Identification of APOBEC3 mutations in cancer genoms
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Organisms :

Group :
Name of Applicant : Vincent CAVAL
Date of application : 17-01-2018
Unit : Molecular Retrovirology
Location : Lwoff 2nd floor room 205
Phone : 0145688365
@ Mail : vincent.caval@pasteur.fr
@ PI-Mail : simon.wain-hobson@pasteur.fr

Project context and summary :

The APOBEC3 proteins (APOBEC3A-H) are single-stranded DNA (ssDNA) cytidine deaminases (CDAs). Those proteins were first tied to innate immunity as antiviral restriction factors as cytidine deamination to uridine results in hypermutation of viral genomes. However APOBEC3 mutaČ›ional signature was recently identified in cancer genomes, suggesting a causal role of APOBEC3 proteins in cancer onset. Accordingly, we demonstrated that both APOBEC3A and APOEC3B proteins can elicit somatic mutations on chromosomal DNA. The aim of this project is to implement in Pasteur’s Galaxy Instance the MutSpec Tool box, allowing the analysis of mutational signature from cancer genomes. This tool will allow to seek and extract APOBEC3 mutational signatures from genomes available in public databases such as TCGA or COSMIC. This tool is also a prerequiste to start implementing NGS sequencing in the lab’s forthcoming work.


Related team publications :
Self-cytoplasmic DNA upregulates the mutator enzyme APOBEC3A leading to chromosomal DNA damage. Suspene et al. Nucleic Acids research. 2017
A prevalent cancer susceptibility APOBEC3A hybrid allele bearing APOBEC3B 3’UTR enhances chromosomal DNA damage. Caval et al, Nature Communication, 2014
Somatic hypermutation of human mitochondrial and nuclear DNA by APOBEC3 cytidine deaminases, a pathway for DNA catabolism. Suspene et al. Plos pathogens. 2011
Service Delivery
Project Manager : fabien.mareuil@pasteur.fr
Project Type : Short
Status : In Progress


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