{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,22]],"date-time":"2025-10-22T17:43:37Z","timestamp":1761155017793},"reference-count":19,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2006,7,17]],"date-time":"2006-07-17T00:00:00Z","timestamp":1153094400000},"content-version":"vor","delay-in-days":4715,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Intl Journal of Cancer"],"published-print":{"date-parts":[[1993,8,19]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Human B\u2010cell lines established from Burkitt lymphoma (BL) and normal B cells immortalized <jats:italic>in vitro<\/jats:italic> by EBV (LCLs) differ in phenotype. While the BL correspond to resting B cells, the LCLs resemble activated B cells. When BLs which have the EBV genome are carried <jats:italic>in vitro<\/jats:italic>, they acquire some of the features of LCLs, such as expression of B\u2010cell activation markers and the tendency to form aggregates. Comparison of several B\u2010cell lines for sensitivity to TGF\u2010\u03b2 showed that the growth of BLs (with few exceptions), but not of the LCLs, was inhibited. The results suggested that the sensitivity to TGF\u2010\u03b2 correlates with the cellular phenotype. In the present work, this assumption is even more critically substantiated by studying 2 sublines of an EBV\u2010genome carrying BL line, Mutu, which were selected for single cells and aggregates. The former (with resting phenotype) was inhibited, while the subline of aggregated cells, which also expressed B\u2010cell activation markers, was not inhibited. Somatic\u2010cell hybrids between BLs, LCLs and non\u2010B cells provided lines with phenotypic differences. Results with a panel of such hybrid lines also showed that those which express the activated B\u2010cell phenotype are not inhibited by TGF\u2010\u03b2. Differences in the levels of expression of activation markers did not influence the response to TGF\u2010\u03b2. \u00a9 1993 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/ijc.2910550124","type":"journal-article","created":{"date-parts":[[2007,2,19]],"date-time":"2007-02-19T23:50:20Z","timestamp":1171929020000},"page":"137-140","source":"Crossref","is-referenced-by-count":9,"title":["Correlation between the growth\u2010inhibitory effect of TGF\u2010\u03b21 and phenotypic characteristics in a panel of B\u2010cell lines"],"prefix":"10.1002","volume":"55","author":[{"given":"Aysin","family":"Altiok","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Barbro","family":"Ehlin\u2010Henriksson","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Eva","family":"Klein","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2006,7,17]]},"reference":[{"key":"e_1_2_1_2_1","doi-asserted-by":"publisher","DOI":"10.1002\/ijc.2910500518"},{"key":"e_1_2_1_3_1","doi-asserted-by":"publisher","DOI":"10.3109\/08977199109000263"},{"key":"e_1_2_1_4_1","doi-asserted-by":"publisher","DOI":"10.1002\/eji.1830170224"},{"key":"e_1_2_1_5_1","doi-asserted-by":"publisher","DOI":"10.1099\/0022-1317-72-12-3025"},{"key":"e_1_2_1_6_1","doi-asserted-by":"publisher","DOI":"10.1038\/349612a0"},{"key":"e_1_2_1_7_1","doi-asserted-by":"publisher","DOI":"10.1099\/0022-1317-71-7-1481"},{"key":"e_1_2_1_8_1","doi-asserted-by":"publisher","DOI":"10.1002\/eji.1830221037"},{"key":"e_1_2_1_9_1","doi-asserted-by":"crossref","first-page":"3855","DOI":"10.4049\/jimmunol.137.12.3855","article-title":"Transforming growth factor\u2010beta, an important immunomodulatory protein for human B lymphocytes","volume":"137","author":"Kehrl J. 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