<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>204(12)</volume><submitter>Kovalchuk AL</submitter><funding>Intramural NIH HHS</funding><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 </pubmed_abstract><journal>The Journal of experimental medicine</journal><pagination>2989-3001</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC2118515</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>AID-deficient Bcl-xL transgenic mice develop delayed atypical plasma cell tumors with unusual Ig/Myc chromosomal rearrangements.</pubmed_title><pmcid>PMC2118515</pmcid><pubmed_authors>duBois W</pubmed_authors><pubmed_authors>McNeil NE</pubmed_authors><pubmed_authors>Janz S</pubmed_authors><pubmed_authors>Mushinski E</pubmed_authors><pubmed_authors>Honjo T</pubmed_authors><pubmed_authors>Kovalchuk AL</pubmed_authors><pubmed_authors>Qi CF</pubmed_authors><pubmed_authors>Ried T</pubmed_authors><pubmed_authors>Potter M</pubmed_authors><pubmed_authors>Li Z</pubmed_authors><pubmed_authors>Muramatsu M</pubmed_authors><pubmed_authors>Hirt C</pubmed_authors><pubmed_authors>Behrens T</pubmed_authors></additional><is_claimable>false</is_claimable><name>AID-deficient Bcl-xL transgenic mice develop delayed atypical plasma cell tumors with unusual Ig/Myc chromosomal rearrangements.</name><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 </description><dates><release>2007-01-01T00:00:00Z</release><publication>2007 Nov</publication><modification>2026-03-16T16:41:08.864Z</modification><creation>2025-08-31T03:08:40.898Z</creation></dates><accession>S-EPMC2118515</accession><cross_references><pubmed>17998390</pubmed><doi>10.1084/jem.20070882</doi></cross_references></HashMap>