D'Emilia J C, Mathey-Prevot B, Jaros K, Wolf B, Steele G, Summerhayes I C
Laboratory of Cancer Biology, New England Deaconess Hospital, Boston, Massachusetts 02115.
Oncogene. 1991 Feb;6(2):303-9.
With the use of viral vectors harboring myc and src oncogenes, we have assessed the potential contribution of these different elements to colonic neoplasia using a transplantation technique resulting in the formation of a heterotopic colon in Wistar Furth rats. While myc alone induced atypia and some dysplasia, src induced focal dysplastic lesions throughout the colon mucosa with evidence of metaplasia. In contrast, lesions induced by myc and src acting cooperatively, were highly dysplastic with evidence of tumor formation after protracted periods. These results indicated the formation of histologically distinct preneoplastic lesions elicited by the action of a single oncogene in colon implants with the production of adenocarcinomas when such oncogenic elements act cooperatively. This model provides an opportunity for studies of the action of different oncogenes, acting singly or in combination, in the multi-step progression to colon tumor formation.
利用携带myc和src癌基因的病毒载体，我们运用一种移植技术在Wistar Furth大鼠体内形成异位结肠，评估了这些不同基因元件对结肠肿瘤形成的潜在作用。单独的myc可诱导细胞异型性和一些发育异常，而src可诱导整个结肠黏膜出现局灶性发育异常病变并有化生迹象。相比之下，myc和src协同作用诱导的病变高度发育异常，长期观察后有肿瘤形成的证据。这些结果表明，在结肠移植物中，单个癌基因的作用可引发组织学上不同的癌前病变，而当这些致癌元件协同作用时则会产生腺癌。该模型为研究不同癌基因单独或联合作用于结肠肿瘤形成的多步骤进程提供了机会。
