@misc{oai:repo.qst.go.jp:00071133,
 author = {Blyth, Benjamin and Kakinuma, Shizuko and Amasaki, Yoshiko and Shang, Yi and Sawai, Tomoko and Hirano, Shinobu and Tsuruoka, Chizuru and Nishimura, Mayumi and Shimada, Yoshiya and et.al and Ｂｌｙｔｈ Ｂｅｎｊａｍｉｎ and 柿沼 志津子 and 甘崎 佳子 and 尚 奕 and 澤井 知子 and 坂入 しのぶ and 鶴岡 千鶴 and 西村 まゆみ and 島田 義也},
 month = {Jun},
 note = {T cell lymphomas in mice can overcome natural tumour barriers via several routes, including deregulation of Bcl11b, Notch, Pten or Ikaros via gene mutation, amplification or loss. Our research has shown that the etiology of T cell lymphomas (e.g. radiation or chemical mutagenesis) is correlated with a pattern in the disruption of the above pathways and how they are activated or inactivated. Carbon ion radiotherapy may be associated with different risks of secondary cancer than conventional photon therapies. A sub-cohort of mice irradiated with 4 or 4.8 Gy carbon ions starting at one week of age (either in a single exposure, or four weekly fractions), was selected for detailed genetic analysis of radiation-induced thymic lymphomas (n = 102 mice). Gross genomic changes at tumour suppressor loci including Pten, Bcl11b and Ikzf1 are being assessed by loss of heterozygosity (LOH) analysis and array-based comparative genome hybridisation. Smaller genetic alterations are being further assessed by exon sequencing of Pten, Bcl11b and Ikzf1 to identify small insertions/deletions and point-mutations. Preliminary results show that although the same pathways are involved in both carbon- and photon radiation-induced tumours, how these pathways are disrupted may be different between radiation types. Mechanistic insight into carbon ion-induced carcinogenesis will be vital in assessing the long-term safety of carbon ion radiotherapy for children., The 6th International Workshop of the Kyoto T Cell Conference},
 title = {Gene signatures in radiation-induced T cell lymphomas.},
 year = {2013}
}