Ootsuyama A, Tanaka K, Tanooka H
Radiobiology Division, National Cancer Center Research Institute, Tokyo.
Jpn J Cancer Res. 1992 Sep;83(9):964-7. doi: 10.1111/j.1349-7006.1992.tb02008.x.
Clonal origin of skin and bone tumors produced by repeated beta-irradiation was determined by using mice with cellular mosaicism created by random X-chromosome inactivation, on the basis of phosphoglycerate kinase-1 (PGK). The backs of female C3H/He (Pgk-1a/Pgk-1b) mice were exposed to beta rays from 90Sr-90Y at a dose of 3 Gy per exposure 3 times weekly until tumors appeared. The cumulative tumor incidence reached 100% 500 days after the beginning of irradiation, as determined by the Kaplan-Meier method. All 8 tumors examined were of a single PGK phenotype: 5 squamous cell carcinomas and 2 osteosarcomas of A-type, and 1 squamous cell carcinoma of B-type. The absence of double PGK phenotype (AB-type) tumors indicated the monoclonal origin of the tumors produced by repeated irradiation.
通过利用基于磷酸甘油酸激酶-1(PGK)随机X染色体失活产生细胞镶嵌性的小鼠,确定了反复β射线照射产生的皮肤和骨肿瘤的克隆起源。雌性C3H/He(Pgk-1a/Pgk-1b)小鼠的背部每周3次接受来自90Sr-90Y的β射线照射,每次照射剂量为3 Gy,直至出现肿瘤。根据Kaplan-Meier方法测定,照射开始后500天累积肿瘤发生率达到100%。所检查的所有8个肿瘤均为单一PGK表型:5个鳞状细胞癌和2个A型骨肉瘤,以及1个B型鳞状细胞癌。不存在双PGK表型(AB型)肿瘤表明反复照射产生的肿瘤起源于单克隆。