The Japan Radiation Research Society Annual Meeting Abstracts
The 49th Annual Meeting of The Japan Radiation Research Society
Session ID : P2-12
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Radiation Effects-Chromosomal Aberration, Carcinogenesis, Genomic Instability
Rag-dependent and Rag-independent pathways for the development of radiation-induced thymic lymphomas in Atm-deficient mice
*Hiroko ISHIIHideo TSUJITomoyasu HIGASHIKouichi TATSHUMITakeshi FURUSEEiko KUBOYuko NODA
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Abstract
We have analyzed the pathway for the development of thymic lymphomas and have identified two pathways, the illegitimate V(D)J recombination and the microhomology-mediated end joining, for the deletion formation of Notch1 gene, which is a major oncogene responsible for the development of thymic lymphomas. In the present study, we examined the induction of thymic lymphomas in Rag2Atm-double deficient mice to elucidate the effect of Atm deficiency on thymic lymphoma induction and to analyze the participation of Rag-mediated pathway for the development of thymic lymphomas in Atm-deficient mice. The Rag2Atm-double deficient mice exhibited the reduced frequencies of spontaneous and radiation-induced thymic lymphomas as compared to those in Atm-deficient mice. The Kaplan-Meier tumor-free survival curve revealed that the induction of thymic lymphomas in Rag2Atm-double deficient mice was significantly delayed as compared to that in Atm-deficient mice. The results indicate that thymic lymphomas are induced via both Rag-dependent and Rag-independent pathways in Atm-deficient mice. The frequencies of Notch1 abnormalities in thymic lymphomas were 30%, 56%, and 46% in Rag2, Atm, and Rag2Atm-double deficient mice, respectively, indicating that Notch1 gene is involved in the development of thymic lymphomas in these mice. It is speculated that the rearrangement of Notch1 gene via Rag-dependent and Rag-independent pathways might participate in the development of thymic lymphomas in Atm-deficient mice.
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© 2006 The Japan Radiation Research Society
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