home > bioproject > PRJEB2036
identifier PRJEB2036
type bioproject
title Study of the cancer genome in T lymphoma showing a recurrent chromosome 12 translocation
description We are studying the “cancer genome” in a cancer prone mouse model: irradiated bloom deficient mice. Loss of the DNA helicase Bloom function has been described in human Bloom syndrome and leads hyper-recombination and cancer predisposition. This gene has been knocked out in mice by the Bradley lab, and like in the human syndrome, bloom deficient mice are cancer prone in a wide variety of different cell types including carcinomas, sarcomas and lymphomas. Thus, this model provides an opportunity to identify genomic regions or genes that are frequently rearranged in cancerWe analyzed a cohort of T lymphoblastic lymphoma primary cell lines derived from the cancer prone Bloom deficient mice using high resolution array CGH and multicolor FISH (collaboration with N- Carter’s group). We discovered, among other alterations in these samples, that the distal part of chromosome 12 was frequently rearranged ( ie deleted or amplified as seen in aCGH and/or translocated seen in MFISH). Chr12 is often involved in balanced and unbalanced translocations in T-lymphoma with different partners (ie:1, 5, 14, 15, 16 and 17) and show frequent rearrangements around E-F2 band (deletion and/or amplifications). Using aCGH and FISH, we were able to map some of these rearrangements and found that a sub-region around 108Mb on chromosome 12 was frequently targeted. • In the cases of unbalanced translocations, in 30% of the cases chromosome 12 breakpoints occur more frequently around 108Mb within a 2.5Mb window (n=15).• In the cases of the balanced translocations, chromosome 12 breakpoints occur within 55Kb around 108Mb in a genomic desert (n=2).• In the cases of the rearrangements on chromosome 12, translocation independent, a 60kb minimum common region containing Bcl11b gene was identified (n=6). We think that the targeted gene in our lymphoma is Bcl11b which is a well know tumour suppressor gene in lymphoma. This gene could be either deleted (by deletion or translocation) or its regulatory element(s) misplaced in the cases of balanced translocations. We need to use genome wide parallel pair-ended sequencing to map more precisely some of the complex breakpoints we have in the balanced and unbalanced translocations involving chromosome 12. Furthermore, we would like to eventually identify any fusion transcript which could arise from these translocations.. This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/
data type Other
Wellcome Sanger Institute
sra-run  ERR008600ERR008601ERR008602ERR008603ERR008604ERR008605ERR008606ERR008607ERR008608ERR008609 More
sra-submission  ERA000204ERA013547
biosample  SAMEA948398SAMEA948394SAMEA948397SAMEA948396SAMEA948393SAMEA948395SAMEA948390SAMEA948392SAMEA948391SAMEA948388 More
sra-sample  ERS001418ERS001421ERS001419ERS001417ERS001420ERS001960ERS002591ERS002592ERS002593ERS002594 More
sra-experiment  ERX002504ERX002502ERX002505ERX002506ERX002503ERX007142ERX007143ERX007137ERX007140ERX007138 More
distribution JSONJSON-LD
status public
visibility unrestricted-access
dateCreated 2010-02-26T00:00:00+0000
dateModified 2010-02-26T00:00:00+0000
datePublished 2010-02-26T00:00:00+0000