Block of T cell development in P53-deficient mice accelerates development of lymphomas with characteristic RAG-dependent cytogenetic alterations

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dc.contributor.authorB B Haines-
dc.contributor.authorChun Jeih Ryu-
dc.contributor.authorS Chang-
dc.contributor.authorA Protopopov-
dc.contributor.authorA Luch-
dc.contributor.authorYun Hee Kang-
dc.contributor.authorD D Draganov-
dc.contributor.authorM F Fragoso-
dc.contributor.authorS G Paik-
dc.contributor.authorHyo Jeong Hong-
dc.contributor.authorR A DePinho-
dc.contributor.authorJ Chen-
dc.date.accessioned2017-04-19T09:04:06Z-
dc.date.available2017-04-19T09:04:06Z-
dc.date.issued2006-
dc.identifier.issn15356108-
dc.identifier.uri10.1016/j.ccr.2006.01.004ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/7294-
dc.description.abstractMice deficient in the DNA damage sensor P53 display normal T cell development but eventually succumb to thymic lymphomas. Here, we show that inactivation of the TCR β gene enhancer (Eβ) results in a block of T cell development at stages where recombination-activating genes (RAG) are expressed. Introduction of the Eβ mutation into p53-/- mice dramatically accelerates the onset of lethal thymic lymphomas that harbor RAG-dependent aberrant rearrangements, chromosome 14 and 12 translocations, and amplification of the chromosomal region 9A1-A5.3. Phenotypic and genetic analyses suggest that lymphomas emerge through a normal thymocyte development pathway. These findings provide genetic evidence that block of lymphocyte development at stages with RAG endonuclease activity can provoke lymphomagenesis on a background with deficient DNA damage responses.-
dc.publisherElsevier-Cell Press-
dc.titleBlock of T cell development in P53-deficient mice accelerates development of lymphomas with characteristic RAG-dependent cytogenetic alterations-
dc.title.alternativeBlock of T cell development in P53-deficient mice accelerates development of lymphomas with characteristic RAG-dependent cytogenetic alterations-
dc.typeArticle-
dc.citation.titleCancer Cell-
dc.citation.number2-
dc.citation.endPage120-
dc.citation.startPage109-
dc.citation.volume9-
dc.contributor.alternativeNameHaines-
dc.contributor.alternativeName류춘제-
dc.contributor.alternativeNameChang-
dc.contributor.alternativeNameProtopopov-
dc.contributor.alternativeNameLuch-
dc.contributor.alternativeName강윤희-
dc.contributor.alternativeNameDraganov-
dc.contributor.alternativeNameFragoso-
dc.contributor.alternativeName백상기-
dc.contributor.alternativeName홍효정-
dc.contributor.alternativeNameDePinho-
dc.contributor.alternativeNameChen-
dc.identifier.bibliographicCitationCancer Cell, vol. 9, no. 2, pp. 109-120-
dc.identifier.doi10.1016/j.ccr.2006.01.004-
dc.description.journalClassY-
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