@misc{oai:repo.qst.go.jp:00071423,
 author = {Ｂｌｙｔｈ, Ｂｅｎｊａｍｉｎ and 森岡, 孝満 and 砂押, 正章 and 島田, 義也 and 柿沼, 志津子 and Ｂｌｙｔｈ Ｂｅｎｊａｍｉｎ and 森岡 孝満 and 砂押 正章 and 島田 義也 and 柿沼 志津子},
 month = {Mar},
 note = {The Pten gene is frequently mutated or lost in radiation-induced T cell lymphomas. Mice with only one copy of Pten are more sensitive to radiation-induced tumours, and mice without Pten activity in developing thymocytes rapidly develop spontaneous T cell lymphoma. 
Yet, it is not clear whether the defect caused by Pten loss/partial loss is due to: 
incorrect development of the T cells prior to irradiation; 
increased radiation damage in Pten-deficient cells; 
faulty post-radiation recovery of the thymus; or, 
whether Pten acts to suppress the growth of radiation-damaged cells over the long term. 
Here, we have used an inducible Pten-knockout model to delete one copy of the Pten gene in mice irradiated with 2.5 Gy X-rays at 7 weeks of age. We have compared groups with Pten deleted at birth, just prior to irradiation, two weeks before irradiation or two weeks after irradiation., 平成25年度個体レベルでのがん研究支援活動ワークショップ},
 title = {Defining the Role of Pten in Radiation-Induced Cancer Susceptibility},
 year = {2014}
}