الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Diffuse large B-cell lymphomas (DLBCL) are the most common type of aggressive B cell non-Hodgkin’s lymphomas.
Using gene expression profiling (GEP), DLBCL NOS can be subdivided into germinal center B-cell (GCB) subtype and activated B-cell (ABC) subtype based on the cell of origin (COO). These two primary subtypes have a high degree of clinical relevance.
Diagnosis relies on a combination of morphologic findings (peripheral blood, bone marrow, or lymph node), immunohistochemistry, immunophenotyping, cytogenetics, fluorescence in situ hybridization (FISH) and molecular genetics.
DLBCL is ideally diagnosed from an excisional biopsy of an abnormally enlarged, suspicious appearing lymph node upon clinical examination and radiographic imaging. Lymph nodes architecture is partially or totally effaced by a diffuse infiltration of medium to large cells with large nucleoli and abundant cytoplasm. The three common morphological variants are; the centroblastic, the immunoblastic and the anaplastic variant.
Polycomb Repressive Complex (PRCs) proteins are transcriptional repressors constituting heterogenous group of protein complexes composed of various combinations of subunits. They act mainly by modifying histones and reduce DNA accessibility.
Enhancer of zeste homolog 2 (EZH2) is the catalytic subunit of the polycomb repressive complex 2 (PRC2) which implements transcriptional repression by trimethylation at lysine 27 of histone H3 (H3K27me3).
On contrary to genetic changes that are non-reversible, epigenetic alterations are reversible. This feature makes epigenetic alterations in cancer an ideal target for developing cancer therapeutics.
Many studies indicate that inhibition of EZH2 results in reduced cancer cell growth and tumor formation so it has obtained significant interest as a potential therapeutic target.