Role of c-MYC, BCL2, and BCL6 Expression in Pathogenesis of Diffuse Large B-Cell Lymphoma

A.E. Misyurina1, V.A. Misyurin2, E.A. Baryakh1, A.M. Kovrigina1, S.K. Kravchenko1

1 Hematology Research Center under the Ministry of Health of the Russian Federation, 4а Novyi Zykovskii pr-d, Moscow, Russian Federation, 125167

2 N.N. Blokhin Russian Cancer Research Center, 24 Kashirskoye sh., Moscow, Russian Federation, 115478

For correspondence: A.E. Misyurina, Graduate student 4а Novyi Zykovskii pr-d, Moscow, Russian Federation, 125167; Tel: +7(909)637-32-49; e-mail:

For citation: Misyurina A.E., Misyurin V.A., Baryakh E.A., Kovrigina A.M., Kravchenko S.K. Role of c-MYC, BCL2, and BCL6 Expression in Pathogenesis of Diffuse Large B-Cell Lymphoma. Klin. Onkogematol. 2014; 7(4): 512–521 (In Russ.).


According to modern concepts based on results of examination of the gene expression profile, there are several subtypes of diffuse large B cell lymphoma (DLBCL): germinal center B cell-like (GCB) and activated B cell-like (ABC) lymphomas. Genes c-MYC, BCL6, and BCL2 are key regulators of B-cell germinal (follicular) differentiation. Genetic abnormalities with their participation are most common in molecular pathogenesis of DLBCL. A total level of activity as well as mechanisms that lead to overexpression each of these genes and production of corresponding proteins have an impact on a disease prognosis. We assume that quantitative assay of c-MYC, BCL6, and BCL2 gene expression, as well as proteins encoded by these genes, can allow to determine high risk DLBCL patients with great accuracy.

Keywords: diffuse large B cell lymphoma, molecular subtypes, risk groups, c-MYC, BCL6, BCL2.

Accepted: September 8, 2014

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