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Native Burkitt's lymphoma (BL) and nasopharyngeal carcinoma (NPC) patients from Kenya were examined with regard to the serum concentrations and distribution of the four IgG subclasses, total IgG, and antibody activities to Epstein-Barr (EB) virus associated antigens. The results were compared with corresponding data of an African control group. As revealed by indirect immunofluorescence techniques, the patients displayed a pattern of IgG and IgA antibodies to EB virus associated antigens which is characteristic for these diseases. No significant differences could be detected between the total lgG levels of the diagnostic groups. The mean total IgG concentrations of our Kenyan patients were two to three times as high as those found in four different groups of Europeans, which is consistent with results of previous studies on Gambian, Nigerian, and Congolese Bantu populations. Quantitative determination of the four IgG subclasses by radial immunodiffusion revealed a unique pattern in the BL group which was characterized by a decreased proportion of IgG2 and significantly lower absolute 1gG2 values as compared with the controls. The IgG subclass distribution pattern in the African NPC sera was essentially identical with that of European NPC and African control sera. The pathogenetic implications of these findings are discussed. [ABSTRACT FROM AUTHOR]

The malignant epithelial cells of two anaplastic EBV-carrying nasopharyngeal carcinomas (NPC) were investigated cytogenetically by Giemsa banding technique. Both tumors had a similar 3q+ marker chromosome with an involvement of band q25, either a duplication of the region q25-q27, or insertion of an unidentified segment at band q25.

The Ig allotype G3m (c3) was numerically more frequent among 70 Kenyan Burkitt lymphoma (BL) cases than in 70 Kenyans with other tumors of the neck (0.02 greater than p greater than 0.01). The distribution of allotypes G1m (a, x) and G3m (b5) did not differ between 50 Caucasian BL cases and blood donors.

Human peripheral lymphocytes from tumor-bearing and non-tumor-bearing patients were added to monolayer cultures of autochthonous and allogeneic normal or neoplastic cells in vitro with or without phytohemagglutinin (PHA). The normal cells were derived from skin, the tumor cells from postnasal carcinomas or sarcomas. The cultures were scored for clearly visible plaques in the monolayer. Without PHA, lymphocytes affected autochthonous skin target cells in 1 of 16 cultures. If PHA was added,the figure increased to nearly 50%(12/28). Whether this phenomenon is related to an autoimmune reaction or to some less specific effect of the PHA stimulus is unknown at present. In the absence of PHA, lymphocytes from African tumor-bearing hosts destroyed allogeneic skin fibroblasts in 4 of 14 cases, and lymphocytes from non-tumor-bearing Swedish donors showed this effect in 14 of 24 tests. The somewhat lower reactivity of the African lymphocytes was also apparent in other tests. It cannot be stated whether the difference was due to the tumor-bearing condition of the hosts or to some other differences involved in comparison of the two groups. Without PHA, lymphocytes of the African tumor patients destroyed their own autochthonous tumor cultures in 4 of 16 cases. Addition of PHA increased the proportion of positives to 20 of 28. A comparison with the corresponding figures for autochthonous skin cultures (1/16 and 12/28, respectively) indicates a relatively higher reactivity against the autochthonous tumor cells, both with and without PHA. This cannot be interpreted as a difference in target cell sensitivity to the same lymphocyte action, because no such difference was apparent when the sensitivity of skin and tumor to allogeneic lymphocytes was compared in the absence of PHA (4/14 and 4/14 with African lymphocyte donors; 14/24 and 14/24 with Swedish lymphocyte donors, respectively). The most probable explanation is that the antigenic barrier responsible for the lymphocyte effect is larger for tumor than for skin, or that the results reflect a presensitization of the tumor donor against its autochthonous neoplastic cells.