{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,21]],"date-time":"2025-10-21T14:57:17Z","timestamp":1761058637521},"reference-count":38,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2006,7,17]],"date-time":"2006-07-17T00:00:00Z","timestamp":1153094400000},"content-version":"vor","delay-in-days":7429,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Intl Journal of Cancer"],"published-print":{"date-parts":[[1986,3,15]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Burkitt's lymphoma (BL) biopsy cells and derived cell lines can be grouped according to their patterns of reactivity with 6 selected monoclonal antibodies (MAbs) against B cell\u2010associated surface antigens. Group I cells react only with MAbs J5 and 38.13, recognising the common acute lymphoblastic leukaemia antigen and a BL\u2010associated antigen respectively; group II cells react with J5 and 38.13 and with one or more of a set of MAbs (Ki\u201024, MHM6, AC2, Ki\u2010I) against \u201clymphoblastoid\u201d antigens; group III cells react only with these anti\u2010\u201clymphoblastoid\u201d MAbs. Tumour biopsy cells from 17 cases of sporadic BL, 9 positive for the Epstein\u2010Barr (EB) virus genome and 8 negative, have been analysed during the process of cell line establishment <jats:italic>in vitro<\/jats:italic>. In early passage the EB virus\u2010negative BL cells showed either a group I phenotype or gave an additional reactivity with MAb Ki\u201024 which placed them in group II; these phenotypes remained essentially stable with continued growth of the cell lines for up to 50 passages. By contrast the EB virus\u2010positive BL cells were much more susceptible to phenotypic change <jats:italic>in vitro<\/jats:italic>. Although such cells displayed a group I or group II phenotype in early passage, many of the lines soon moved into group III whilst retaining the karyotypic markers indicative of their malignant origin. These observations suggest that a resident EB virus genome can drive the <jats:italic>in vitro<\/jats:italic> progression of BL cells towards a more \u201clymphoblastoid\u201d phenotype. This was confirmed in subsequent experiments where virus\u2010negative BL cell lines were converted to EB virus positivity by <jats:italic>in vitro<\/jats:italic> infection. Clearly, therefore, phenotypic analysis of long\u2010established lines can lead to false distinctions being drawn between the EB virus\u2010positive and \u2010negative forms of sporadic BL; both may derive from the same sub\u2010population of target B cells <jats:italic>in vivo<\/jats:italic>.<\/jats:p>","DOI":"10.1002\/ijc.2910370307","type":"journal-article","created":{"date-parts":[[2007,2,19]],"date-time":"2007-02-19T20:24:12Z","timestamp":1171916652000},"page":"367-373","source":"Crossref","is-referenced-by-count":70,"title":["Epstein\u2010Barr virus status and tumour cell phenotype in sporadic Burkitt's lymphoma"],"prefix":"10.1002","volume":"37","author":[{"given":"M.","family":"Rowe","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"C. M.","family":"Rooney","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"C. 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