The Japan Radiation Research Society Annual Meeting Abstracts
The 52nd Annual Meeting of the Japan Radiation Research Society
Session ID : OC-13
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Carcinogenesis 2
The role of Rev1 in radiation and chemical -induced thymic lymphoma development using Rev1 Tg mice
*Megumi TOYOSHIMAYang XITakahiro KIKAMOTOHiromitsu WATANABEHiroaki HONDAKanya HAMASAKIYoichiro KUSUNOKIYuji MASUDAKenji KAMIYA
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Abstract
Ionizing radiation is a carcinogenic agent. Radiation carcinogenesis is the results of a series of somatic mutations. Translesion DNA synthesis (TLS) is known as error-prone DNA repair. Y family DNA polymerases which operate TLS can bypass a various damage lesions with low fidelity. Y family DNA polymerase is responsible for spontaneous and damage-induced mutagenesis.
Rev1 is one of Y family DNA polymerase and has a regulatory role in TLS. However, little is known whether Rev1 protein has the precise role in tumor formation in vivo.
We generated Rev1 transgenic mice (Rev1 Tg mice) that continuously express a Rev1transgene in various tissues. Both Rev1 Tg and wild-type (Wt) mice were subjected to Υ-irradiation of 1.6Gy four times at a weekly internal, starting at the age of 4 weeks. Rev1 Tg and wild type mice (C57BL/6) were treated with the mutagenic agent N-methyl-N-nitrosourea (MNU) through intraperitoneal injection and examined their development of tumor.
Most mice were died because of thymic lymphoma among all developed tumors deduced from MNU treatment. Compared with wild type mice, Rev1 Tg mice showed the rapid and high tendency of thymic lymphoma development. On the other hand, overexpression of Rev1 prolonged radiation-induced thymic lymphoma development.
These findings demonstrate that overexpression of Rev1 may be associated with chemical and raditation-induced tumorigenesis with the different mechanism.
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© 2009 The Japan Radiation Research Society
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