Direct single gene mutational events account for radiation-induced intestinal adenoma yields in Apcmin/+ mice
Direct single gene mutational events account for radiation-induced intestinal adenoma yields in Apcmin/+ mice
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DOI：
10.1667/rr3335
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发表时间：
2005-05-01
影响因子：
3.4
通讯作者：
Cox, R
中科院分区：
文献类型：
--
作者：
Ellender, M;Harrison, JD;Cox, R
报道了X射线照射诱发APC(Min/+)小鼠小肠肿瘤(主要是腺瘤)的资料。将这些发生率与文献中对辐射诱导的直接单基因突变频率的估计进行比较，支持这样的假设，即APC(+)的直接突变丢失是腺瘤发生的唯一条件。此外，在该动物模型中，辐射诱导的每个靶干细胞引发腺瘤的估计与辐射诱导的直接体细胞基因突变频率相似或更低。因此，虽然这里报道的数据不排除基因组不稳定性在肿瘤进展中的作用，但在这个模型中，没有必要假设辐射诱导的可传递基因组不稳定性参与了肠腺瘤的发生。(C)2005年，由辐射研究学会提供。
Data on the induction of small intestinal tumors, predominantly adenomas, by X radiation in Apc(Min/+) mice are reported. Comparison of these incidences with estimates of radiation-induced direct single gene mutation frequencies taken from the literature support the hypothesis that direct mutational loss of Apc(+) is the sole requirement for initiation of adenoma. Furthermore, estimates of radiation-induced initiation of adenoma per target stem cell in this animal model are similar to or less than radiation-induced direct somatic gene mutation frequencies. Therefore, while the data reported here do not preclude a role for genomic instability in tumor progression, it is not necessary in this model to postulate the involvement of radiation-induced transmissible genomic instability in initiation of intestinal adenoma. (c) 2005 by Radiation Research Society.