Saggioro D, Zamarchi R, D'Andrea E, Chieco-Bianchi L
Institute of Oncology, University of Padova, Italy.
Br J Cancer. 1988 Aug;58(2):152-7. doi: 10.1038/bjc.1988.183.
Cell lines derived from A-MuLV induced thymic lymphomas in BALB/c and C57BL/6 mice were analysed for their in vivo and in vitro potential of growth. Despite their immunogenicity, cell lines of BALB/c origin readily grew in syngeneic recipients. On the contrary, all cell lines of C57BL/6 origin failed to grow in immunocompetent hosts even though they were able to form tumours in immunosuppressed syngeneic mice. Among C57BL/6 lymphoma cells progression toward a more malignant phenotype was observed in TB6-3 cells, and in their derived clones, after several in vitro passages. This event was accompanied by the in vitro loss of requirement for exogenous growth factor(s) when tumorigenic TB6-3 cells were plated at high density. Moreover, culture medium from fully malignant TB-3 cells was mitogenic for mature T-lymphoma cells suggesting the involvement of an autocrine mechanism in the control of cell proliferation. Apparently, the viral oncogene (v-abl) is not directly involved in malignant progression since no differences between nontumorigenic and tumorigenic cells could be detected in A-MuLV integration patterns, v-abl specific mRNA expression, and P160gag-abl production.
对源自A-MuLV诱导的BALB/c和C57BL/6小鼠胸腺淋巴瘤的细胞系进行了体内和体外生长潜力分析。尽管具有免疫原性，但源自BALB/c的细胞系能在同基因受体中轻松生长。相反，所有源自C57BL/6的细胞系在免疫功能正常的宿主中均无法生长，尽管它们能够在免疫抑制的同基因小鼠中形成肿瘤。在C57BL/6淋巴瘤细胞中，TB6-3细胞及其衍生克隆在多次体外传代后出现了向更恶性表型的进展。当致瘤性TB6-3细胞以高密度接种时，这一事件伴随着体外对外源生长因子需求的丧失。此外，完全恶性的TB-3细胞的培养基对成熟T淋巴瘤细胞具有促有丝分裂作用，提示自分泌机制参与细胞增殖的调控。显然，病毒癌基因（v-abl）并不直接参与恶性进展，因为在A-MuLV整合模式、v-abl特异性mRNA表达和P160gag-abl产生方面，未检测到非致瘤性细胞和致瘤性细胞之间存在差异。
