{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["204(12)"],"submitter":["Kovalchuk AL"],"funding":["Intramural NIH HHS"],"pubmed_abstract":["Activation-induced cytidine deaminase (AID) is required for immunoglobulin (Ig) class switch recombination and somatic hypermutation, and has also been implicated in translocations between Ig switch regions and c-Myc in plasma cell tumors in mice. We asked if AID is required for accelerated tumor development in pristane-treated Bcl-xL transgenic BALB/c mice deficient in AID (pBxAicda-/-). pBxAicda-/- mice developed tumors with a lower frequency (24 vs. 62%) and a longer mean latency (108 vs. 36 d) than AID-sufficient mice. The tumors appeared in oil granuloma tissue and did not form ascites. By interphase fluorescence in situ hybridization, six out of nine pBxAicda-/- primary tumors had T(12;15) and one had T(6;15) chromosomal translocations. Two tumors were transplantable and established "],"journal":["The Journal of experimental medicine"],"pagination":["2989-3001"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC2118515"],"repository":["biostudies-literature"],"pubmed_title":["AID-deficient Bcl-xL transgenic mice develop delayed atypical plasma cell tumors with unusual Ig/Myc chromosomal rearrangements."],"pmcid":["PMC2118515"],"pubmed_authors":["duBois W","McNeil NE","Janz S","Mushinski E","Honjo T","Kovalchuk AL","Qi CF","Ried T","Potter M","Li Z","Muramatsu M","Hirt C","Behrens T"],"additional_accession":[]},"is_claimable":false,"name":"AID-deficient Bcl-xL transgenic mice develop delayed atypical plasma cell tumors with unusual Ig/Myc chromosomal rearrangements.","description":"Activation-induced cytidine deaminase (AID) is required for immunoglobulin (Ig) class switch recombination and somatic hypermutation, and has also been implicated in translocations between Ig switch regions and c-Myc in plasma cell tumors in mice. We asked if AID is required for accelerated tumor development in pristane-treated Bcl-xL transgenic BALB/c mice deficient in AID (pBxAicda-/-). pBxAicda-/- mice developed tumors with a lower frequency (24 vs. 62%) and a longer mean latency (108 vs. 36 d) than AID-sufficient mice. The tumors appeared in oil granuloma tissue and did not form ascites. By interphase fluorescence in situ hybridization, six out of nine pBxAicda-/- primary tumors had T(12;15) and one had T(6;15) chromosomal translocations. Two tumors were transplantable and established ","dates":{"release":"2007-01-01T00:00:00Z","publication":"2007 Nov","modification":"2026-03-16T16:41:08.864Z","creation":"2025-08-31T03:08:40.898Z"},"accession":"S-EPMC2118515","cross_references":{"pubmed":["17998390"],"doi":["10.1084/jem.20070882"]}}