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源自艾贝尔逊鼠白血病病毒诱导的胸腺淋巴瘤的细胞的体外恶性进展。

In vitro malignant progression of cells derived from Abelson murine leukaemia virus-induced thymic lymphomas.

作者信息

Saggioro D, Zamarchi R, D'Andrea E, Chieco-Bianchi L

机构信息

Institute of Oncology, University of Padova, Italy.

出版信息

Br J Cancer. 1988 Aug;58(2):152-7. doi: 10.1038/bjc.1988.183.

Abstract

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.

摘要

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。

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