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Distinctions between endemic and sporadic forms of epstein-barr virus-positive burkitt's lymphoma

✍ Scribed by M. Rowe; C. M. Rooney; A. B. Rickinson; G. M. Lenoir; H. Rupani; D. J. Moss; H. Stein; M. A. Epstein


Publisher
John Wiley and Sons
Year
1985
Tongue
French
Weight
822 KB
Volume
35
Category
Article
ISSN
0020-7136

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✦ Synopsis


Abstract

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 iso‐type 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 cumps 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‐11 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.


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