{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,13]],"date-time":"2026-02-13T08:07:45Z","timestamp":1770970065814,"version":"3.50.1"},"reference-count":35,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2006,7,18]],"date-time":"2006-07-18T00:00:00Z","timestamp":1153180800000},"content-version":"vor","delay-in-days":5018,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Intl Journal of Cancer"],"published-print":{"date-parts":[[1992,10,21]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Burkitt lymphoma (BL) cell lines which retain the phenotypic characteristics of the freshly\u2010isolated tumour cells (group I cells) readily enter programmed cell death (apoptosis) in response to a variety of triggers. By contrast, isogenic BL cells which are phenotypically altered as a result of activation of their resident EBV genome (group\u2010III cells) are highly protected from apoptosis. Phenotypic changes in group\u2010III cells include the up\u2010regulation of the oncogene, <jats:italic>bcl<\/jats:italic>\u20102. Expression of the 26\u2010kDa <jats:italic>bcl<\/jats:italic>\u20102 protein in group\u20101 BL cells following gene transfer was found to afford protection from apoptosis: the degree of protection was proportional to the amount of <jats:italic>bcl<\/jats:italic>\u20102 protein expressed. When group\u20101 <jats:italic>bcl<\/jats:italic>\u20102 transfectants were compared with their group\u2010III counterparts it was found that, whilst <jats:italic>bcl<\/jats:italic>\u20102 made a significant contribution in protecting from entry into apoptosis, hyper\u2010expression of <jats:italic>bcl<\/jats:italic>\u20102 protein in group\u20101 cells (well beyond that of group\u2010III cells) was necessary to attain the high levels of protection observed in group\u2010III cells. These results suggested that additional, <jats:italic>bcl<\/jats:italic>\u20102\u2010independent, survival mechanisms could operate in BL cells. In support of this notion it was also found that: (I) prolonged culture of group\u20101 lines <jats:italic>in vitro<\/jats:italic> resulted in enhanced survival in the absence of <jats:italic>bcl<\/jats:italic>\u20102 up\u2010regulation, and (2) exposure of group\u20101 cells to interferon\u2010\u03b1 triggered a <jats:italic>bcl<\/jats:italic>\u20102\u2010independent protective response. The molecular mechanisms of both the <jats:italic>bcl<\/jats:italic>\u20102\u2010dependent and \u2010independent survival pathways remain to be determined. \u00a9 1992 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/ijc.2910520424","type":"journal-article","created":{"date-parts":[[2007,2,19]],"date-time":"2007-02-19T22:50:29Z","timestamp":1171925429000},"page":"636-644","source":"Crossref","is-referenced-by-count":54,"title":["Prevention of programmed cell death in burkitt lymphoma cell lines by <i>bcl<\/i>\u20102\u2010dependent and \u2010independent mechanisms"],"prefix":"10.1002","volume":"52","author":[{"given":"Anne E.","family":"Milner","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gerald D.","family":"Johnson","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Christopher D.","family":"Gregory","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2006,7,18]]},"reference":[{"key":"e_1_2_1_2_1","first-page":"1915","article-title":"Constitutive c\u2010nzyc expression in an IL\u20103\u2010dependent myeloid cell line suppresses cell\u2010cycle arrest and accelerates apoptosis.","volume":"6","author":"Askew D. 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