The normal counterpart of the neoplastic B cells occurring in Burkitt's lymphomas (BL) is an issue of controversial debate. To clarify this matter, a semi-nested primer polymerase chain reaction was performed to amplify the VDJ rearrangements of the immunoglobulin heavy chain (VH) gene of DNA extracts from 10 (8 sporadic and 2 endemic) BL cases. The resulting amplificates were sequenced for comparison with known germ line VH segments. The control cases comprised six cases of B cell chronic lymphocytic leukemia and six cases of mantle cell lymphoma known to display naive nonmutated, ie, pre-germinal center VH configurations; and eight cases offollicular center lymphoma known to display mutated VH genes with signs of a still-ongoing mutation reaction, characteristic for germinal center cells and lymphomas that derive therefrom. The results of this approach revealed that both sporadic and endemic BL express mutated Vff genes with a mutation frequency considerably lower (4.9% and 5.4%, respectively) than that observed infollicular center lymphoma (11.8%). In addition, after subcloning the amplificates, sequence analysis revealed no signs of ongoing mutations. These results led us to conclude that the derivation of neoplastic B cells in BL is definitely not from naive, nonmutated pregerminal center B cells. Instead, our findings support the view that BL cells stem either from early centroblasts that are arrested after an inilial hypermutation reaction, or front germinal center B cells that have differentiated in terms of surface immunoglobulin profile and mutation pattern but not in terms of morphology and proliferation toward SIgM+ IgD- memory B cells because of the deregulated c-myc gene expression.

Tamaru, J., Hummel, M., Marafioti, T., Kalvelage, B., Leoncini, L., Minacci, C., et al. (1995). Burkitt's lymphomas express vh genes with a moderate number of antigen-selected somatic mutations. THE AMERICAN JOURNAL OF PATHOLOGY, 147(5), 1398-1407.

Burkitt's lymphomas express vh genes with a moderate number of antigen-selected somatic mutations

LEONCINI L.;TOSI P.;
1995-01-01

Abstract

The normal counterpart of the neoplastic B cells occurring in Burkitt's lymphomas (BL) is an issue of controversial debate. To clarify this matter, a semi-nested primer polymerase chain reaction was performed to amplify the VDJ rearrangements of the immunoglobulin heavy chain (VH) gene of DNA extracts from 10 (8 sporadic and 2 endemic) BL cases. The resulting amplificates were sequenced for comparison with known germ line VH segments. The control cases comprised six cases of B cell chronic lymphocytic leukemia and six cases of mantle cell lymphoma known to display naive nonmutated, ie, pre-germinal center VH configurations; and eight cases offollicular center lymphoma known to display mutated VH genes with signs of a still-ongoing mutation reaction, characteristic for germinal center cells and lymphomas that derive therefrom. The results of this approach revealed that both sporadic and endemic BL express mutated Vff genes with a mutation frequency considerably lower (4.9% and 5.4%, respectively) than that observed infollicular center lymphoma (11.8%). In addition, after subcloning the amplificates, sequence analysis revealed no signs of ongoing mutations. These results led us to conclude that the derivation of neoplastic B cells in BL is definitely not from naive, nonmutated pregerminal center B cells. Instead, our findings support the view that BL cells stem either from early centroblasts that are arrested after an inilial hypermutation reaction, or front germinal center B cells that have differentiated in terms of surface immunoglobulin profile and mutation pattern but not in terms of morphology and proliferation toward SIgM+ IgD- memory B cells because of the deregulated c-myc gene expression.
1995
Tamaru, J., Hummel, M., Marafioti, T., Kalvelage, B., Leoncini, L., Minacci, C., et al. (1995). Burkitt's lymphomas express vh genes with a moderate number of antigen-selected somatic mutations. THE AMERICAN JOURNAL OF PATHOLOGY, 147(5), 1398-1407.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11365/9466
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