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Haines, Brian B.,Ryu, Chun Jeih,Chang, Sandy,Protopopov, Alexei,Luch, Andreas,Kang, Yun Hee,Draganov, Dobrin D.,Fragoso, Maria F.,Paik, Sang Gi,Hong, Hyo Jeong,DePinho, Ronald A.,Chen, Jianzhu Cell Press 2006 CANCER CELL Vol.9 No.2
<P><B>Summary</B></P><P>Mice 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 <I>p53<SUP>−/−</SUP></I> 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.</P>