Kuzumaki N, Kobayashi H
Cancer Res. 1975 Jul;35(7):1718-22.
The WKA/Mk rat tumors induced by Friend virus complex, Rauscher virus complex, and their associated lymphatic leukemia viruses were investigated for their antigenic relationhips with transplantation experiments and cytotoxicity tests. It was found that Friend lymphatic leukemia virus-induced tumors lacked part of the tumor-associated transplantation antigens (TATA's) on Friend virus complex-induced tumors, and the former did not express the type-specific (Friend) TATA for the latter not shared by Rauscher virus complex-induced tumors, which was previously reported by the authors. In contrast, the antigenic differences between TATA's of Rauscher virus complex-induced tumors and those of Rauscher lymphatic leukemia virus-induced tumors were not clearly demonstrated. Furthermore, these studies indicated that Rauscher lymphatic leukemia virus-induced tumors had a weak type-specific TATA not shared by the tumors induced by Friend lymphatic leukemia virus. These results of transplantation studies were also serologically supported by cytotoxicity tests.
利用移植实验和细胞毒性试验,对由弗氏病毒复合体、劳氏病毒复合体及其相关淋巴白血病病毒诱导的WKA/Mk大鼠肿瘤的抗原关系进行了研究。结果发现,弗氏淋巴白血病病毒诱导的肿瘤缺乏弗氏病毒复合体诱导肿瘤上的部分肿瘤相关移植抗原(TATA),并且前者不表达后者的型特异性(弗氏)TATA,劳氏病毒复合体诱导的肿瘤不具有该型特异性TATA,这是作者之前报道过的。相比之下,劳氏病毒复合体诱导肿瘤的TATA与劳氏淋巴白血病病毒诱导肿瘤的TATA之间的抗原差异并未得到明确证实。此外,这些研究表明,劳氏淋巴白血病病毒诱导的肿瘤具有一种弱的型特异性TATA,弗氏淋巴白血病病毒诱导的肿瘤不具有该型特异性TATA。移植研究的这些结果也得到了细胞毒性试验的血清学支持。