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以携带ｖ－ｆｅｓ癌基因的Ｓｎｙｄｅｒ－Ｔｈｅｉｌｅｎ猫科肉瘤病毒（ｆｅｌｉｎｅｓａｒｃｏｍａｖｉｒｕｓｏｆＳｎｙｄｅｒ－Ｆｈｅｉｌｅｎｓｔｒａｉｎ，ＳＴ－ＦｅＳＶ）接种１０８只Ｗｉｓｔａｒ／Ｍａ纯系大鼠新生幼鼠。其中６６例接种后６０天内于接种部位出现肿瘤（Ａ组），１７例１１７ｄ后出现肿瘤（Ｂ组），１７例出现血管瘤样纤维性病变（Ｃ组）。Ａ、Ｂ二组出现肺或其他远隔脏器的转移率分别为５９１％、１１８％，二者差异显著，表明Ａ组肉瘤恶性程度高于Ｂ组。通过原位杂交，免疫组织化学染色，多聚酶链反应单链构象多形性分析，ＤＮＡ序列分析及血清抗Ｐ８５抗体的检测表明：ｖ－ｆｅｓ癌基因信号出现于多数Ａ组肉瘤细胞，部分Ｂ组肉瘤细胞及少数Ｃ组增生血管内皮细胞。Ａ组肉瘤中ｖ－ｆｅｓ基因产物Ｐ８５表达程度明显高于Ｂ组，而良性病变（Ｃ组）中未见表达。ｖ－ｆｅｓ癌基因突变率Ａ组肉瘤明显低于Ｂ组肉瘤，Ｂ组则明显低于Ｃ组。Ａ组例中血清抗Ｐ８５特异抗体在阳转于瘤结节检出之后，而Ｂ组例中则阳转于瘤结节检出之前。提示肿瘤的恶性程度有赖于癌基因及其所决定的基因产物的有效表达，基因的有效表达则由其完整程度所决定
108 Wistar / Ma pure newborn rat pups were inoculated with Snyder-Theilen feline sarcoma virus (ST-FeSV) carrying v-fes oncogene. Sixty-six of them showed tumor at inoculation site 60 days after inoculation (group A), 17 cases developed tumor after 117 days (group B), and 17 cases showed hemangioma-like fibrosis (group C). The metastatic rates of lung or other distant organs in groups A and B were 591% and 118%, respectively, showing significant differences between the two groups, indicating that the malignancy of group A was higher than that of group B. By in situ hybridization, immunohistochemical staining, single strand conformation polymorphism of the polymerase chain reaction, DNA sequence analysis and detection of serum anti-P85 antibody showed: v-fes oncogene signal appeared in most A group of sarcoma cells, part of the B group Sarcoma cells and a few C group of hyperplastic vascular endothelial cells. The expression of v-fes gene product P85 in group A sarcoma was significantly higher than that in group B, but not in group C (benign lesions). The mutation rate of v-fes oncogene in Group A was significantly lower than that in Group B, but in Group B was significantly lower than that in Group C. In group A, the serum anti-P85 specific antibody was detected after the positive rotation in the nodule, while in the group B, the positive rotation was detected before the nodules were detected. Suggesting that the degree of malignancy depends on the cancer gene and the gene expression of the effective expression of the effective expression of the gene by its completeness of the decision