Rowe M, Rooney C M, Rickinson A B, Lenoir G M, Rupani H, Moss D J, Stein H, Epstein M A
Int J Cancer. 1985 Apr 15;35(4):435-41. doi: 10.1002/ijc.2910350404.
Tumour cell lines were established in vitro from 16 cases of Epstein-Barr (EB) virus genome-positive Burkitt's lymphoma (BL), 7 of "endemic" origin (i.e. from holoendemic malarial areas of Africa and of New Guinea) and 9 of "sporadic" origin (i.e. from outside such high-incidence areas). All the BL cell lines thus established were monoclonal by immunoglobulin isotype expression and displayed a characteristic chromosomal translocation, t(8:14) or t(8:22), confirming their malignant origin. Clear differences observed between the individual BL cell lines appeared to be related to their endemic or sporadic status. All 7 endemic cell lines began growth as a carpet of single cells, often with small, loose clumps appearing in later passage. Whilst 3 lines of sporadic origin displayed a similar pattern to the above, the majority of sporadic lines grew as large, tight clumps of cells from the first passage onwards. These differences in growth pattern were reflected by differences in cell surface phenotype, as defined in indirect immunofluorescence tests using a panel of monoclonal antibodies (MAbs) specific for B-lineage-associated antigens. BL cell lines could be classified into 3 separate groups on the basis of their reactivity with 6 particular antibodies (MHM6, AC2, Ki-1, Ki-24, J5 and 38.13). All 7 endemic BL cell lines and 2 of the 3 sporadic BL cell lines which began growth as single cells showed a group-I cell-surface phenotype (MHM6, AC2, Ki-1, Ki-24 negative; J5, 38.13 positive) in early passage. In contrast, all 6 sporadic BL cell lines which began growth in large clumps displayed a distinct group-II phenotype (MHM6, AC2, Ki-1 positive/negative; Ki-24, J5, 38.13 positive); in later passage most of these sporadic lines progressed to a group-III phenotype (MHM6, AC2, Ki-1, Ki-24 positive; J5, 38.13 negative) without loss of those immunoglobulin and chromosomal markers identifying the cells' malignant origin. These clear differences between endemic BL cell lines on the one hand and the majority of sporadic BL cell lines on the other suggest that endemic BL arises from a more restricted range of progenitor B cells than does the sporadic form of the disease.
从16例爱泼斯坦 - 巴尔(EB)病毒基因组阳性的伯基特淋巴瘤(BL)患者体内建立了肿瘤细胞系,其中7例源于“地方性”(即来自非洲和新几内亚的高度地方性疟疾地区),9例源于“散发性”(即来自此类高发病率地区以外)。通过免疫球蛋白同种型表达确定,所有由此建立的BL细胞系均为单克隆性,并显示出特征性的染色体易位,t(8:14)或t(8:22),证实了它们的恶性起源。在各个BL细胞系之间观察到的明显差异似乎与其地方性或散发性状态有关。所有7个地方性细胞系最初以单细胞层的形式生长,在传代后期常常出现小的、松散的细胞团。虽然3个散发性起源的细胞系表现出与上述相似的模式,但大多数散发性细胞系从第一代开始就以大的、紧密的细胞团形式生长。这些生长模式的差异通过细胞表面表型的差异得以体现,细胞表面表型是通过使用一组针对B系相关抗原的单克隆抗体(MAb)进行间接免疫荧光试验来定义的。根据BL细胞系与6种特定抗体(MHM6、AC2、Ki-1、Ki-24、J5和38.13)的反应性,可将其分为3个不同的组。所有7个地方性BL细胞系以及3个最初以单细胞形式生长的散发性BL细胞系中的2个,在传代早期显示出I组细胞表面表型(MHM6、AC2、Ki-1、Ki-24阴性;J5、38.13阳性)。相比之下,所有6个最初以大细胞团形式生长的散发性BL细胞系显示出独特的II组表型(MHM6、AC2、Ki-1阳性/阴性;Ki-24、J5、38.13阳性);在传代后期,这些散发性细胞系中的大多数进展为III组表型(MHM6、AC2、Ki-1、Ki-24阳性;J5、38.13阴性),同时并未丧失那些识别细胞恶性起源的免疫球蛋白和染色体标记。一方面地方性BL细胞系与另一方面大多数散发性BL细胞系之间的这些明显差异表明,与散发性疾病形式相比,地方性BL起源于范围更有限的祖B细胞。