The molecular pathogenesis of B-cell non-Hodgkin lymphoma.

Autor: Blombery PA; Peter MacCallum Cancer Centre, Melbourne, Vic., Australia., Wall M; Victorian Cancer Cytogenetics Service, St Vincent's Hospital Melbourne, University of Melbourne, Fitzroy, Vic., Australia., Seymour JF; Peter MacCallum Cancer Centre, Melbourne, Vic., Australia.
Jazyk: angličtina
Zdroj: European journal of haematology [Eur J Haematol] 2015 Oct; Vol. 95 (4), pp. 280-93. Date of Electronic Publication: 2015 Jun 09.
DOI: 10.1111/ejh.12589
Abstrakt: The B-cell non-Hodgkin lymphomas (B-NHL) are a diverse group of haematological malignancies which arise from the mature B-lymphocyte compartment. Recently, our understanding of the molecular pathogenesis of these disorders has greatly increased due to technological advances such as high-throughput DNA sequencing techniques. A paradigm of B-NHL pathogenesis has emerged where the normal genetic processes that are central to generating B-cell receptor diversity (somatic hypermutation and class switch/VDJ recombination) also drive the genesis of large-scale, chromosomal-level genetic lesions and smaller-scale gene-level mutations to produce the malignant phenotypes observed. Whilst a significant degree of genetic heterogeneity exists within each B-NHL subtype, the genetic lesions present within each subtype show a degree of convergence on common intracellular signalling, epigenetic and cell cycle pathways. This convergence gives an insight into the key oncogenic drivers of specific B-NHL subtypes and potential targets for therapeutic intervention. This review covers the current understanding of the causative genetic processes of B-NHL, the associated driving molecular lesions and the implications of these findings for the treatment of this group of disorders.
(© 2015 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)
Databáze: MEDLINE
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