Pathogenesis of Non-Hodgkin's Lymphoma

2011 ◽  
Vol 29 (14) ◽  
pp. 1803-1811 ◽  
Author(s):  
Hendrik Nogai ◽  
Bernd Dörken ◽  
Georg Lenz

The understanding of the molecular pathogenesis of non-Hodgkin's lymphomas (NHL) has significantly improved in recent years. Advances in molecular biology and genetics lead to the identification and characterization of several oncogenic pathways involved in lymphomagenesis. This knowledge will ultimately lead to improved diagnostic and therapeutic strategies for patients with NHL. This review summarizes current concepts of the molecular pathogenesis of the most common NHL subtypes, with a special emphasis on diffuse large B-cell lymphoma, the most common lymphoma subtype.

2005 ◽  
Vol 23 (26) ◽  
pp. 6351-6357 ◽  
Author(s):  
Izidore S. Lossos

Diffuse large B-cell lymphoma (DLBCL) is a heterogeneous clinicopathologic entity accounting for 30% of non-Hodgkin's lymphomas. The pathogenesis of DLBCL is complex and heterogeneous. Recent studies using analysis of global gene expression with DNA microarrays and the classical molecular approaches demonstrate presence of several DLBCL subtypes characterized by different cells of origin, cytogenetic and molecular aberrations, and distinct pathogenesis. This review summarizes the progress in understanding of DLBCL biology and presents a state-of-the-art overview of DLBCL molecular pathogenesis.


2017 ◽  
Vol 59 (7) ◽  
pp. 1710-1716 ◽  
Author(s):  
Darius Juskevicius ◽  
Anne Müller ◽  
Hind Hashwah ◽  
Pontus Lundberg ◽  
Alexandar Tzankov ◽  
...  

Blood ◽  
1997 ◽  
Vol 90 (3) ◽  
pp. 1168-1174 ◽  
Author(s):  
Outi Monni ◽  
Heikki Joensuu ◽  
Kaarle Franssila ◽  
Juha Klefstrom ◽  
Kari Alitalo ◽  
...  

Abstract Gene activation by translocation between an oncogene and an immunoglobulin heavy-chain gene, which leads to increased expression of the oncoprotein, is a well-known mechanism in the genesis of B-cell lymphomas. In contrast, the role of gene amplification in activation of oncogenes in non-Hodgkin's lymphomas is poorly characterized. To study the BCL2 amplification we performed comparative genomic hybridization (CGH), Southern blot hybridization, Western analysis, immunohistochemistry, metaphase fluorescence in situ hybridization, and chromosome analysis on 26 cases of diffuse large B-cell lymphoma (large noncleaved cell lymphoma). The gain or high-level amplification of 18q was found in eight tumors (31%) by CGH, and Southern analysis revealed BCL2 amplification in these cases, but not in the cases with normal chromosome 18 or t(14; 18)(q32; q21). Western immunoblot analysis and immunohistochemistry revealed a high-level expression of BCL2 protein in the cases with BCL2 amplification and t(14; 18)(q32; q21). However, translocation (14; 18)(q32; q21) was not detected in any of the cases with BCL2 amplification. Therefore, our results suggest that amplification of the BCL2 gene is an important mechanism for BCL2 protein overexpression in diffuse large B-cell lymphoma.


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