Mechanistically, EZH2 specifically stabilizes the chromatin accessibility of a cluster of genes that are important for T<sub>FH</sub> fate commitment, particularly B cell lymphoma 6 (Bcl6), and thus directs T<sub>FH</sub> cell commitment.
We identified 122 patients diagnosed as having large B-cell lymphoma (44, MYC-negative; 29, MYC-EC; 23, MYC rearrangement; 22, MYC and BCL2 rearrangements; 4, MYC, BCL2, and BCL6 rearrangements). p53 expression significantly correlated with DLBCL with abnormal MYC status (MYC-EC, MYC rearrangement, and MYC overexpression), but adverse p53 prognostic effect was only seen with MYC-rearranged lymphoma.
B-cell lymphoma-6 (Bcl6) is a transcriptional repressor that plays important roles in various physiological activities such as innate and adaptive immune response, lymphocyte differentiation, and cell cycle regulation in mammals.
Multiple genetic aberrations in the regulation of BCL6, including in acetyltransferase genes, occur in clinically aggressive B-cell lymphomas and lead to higher expression levels and activity of this transcriptional repressor.
We underscore the critical importance of BCL6 and its associated epigenetic programs in the development of B-cell lymphoma, and discuss avenues for the therapeutic targeting of BCL6 in this context.
The transcriptional corepressor B-cell lymphoma 6 (BCL6) is a member of the Broad-complex, Tramtrack, and Bric-abrac/poxvirus and zinc finger (BTB/POZ) transcription factor family and master regulator of the immune cells in the GC reaction.
The rearrangement of immunoglobulin loci during the germinal center reaction is associated with an increased risk of chromosomal translocations that activate oncogenes such as MYC, BCL2 or BCL6, thus contributing to the development of B-cell lymphomas.
B-lymphocyte-induced maturation protein-1 (Blimp1), a transcriptional repressor of negative regulators of osteoclastogenesis, was also downregulated by Ambn, resulting in the elevated expression of v-maf musculoaponeurotic fibrosarcoma oncogene family, protein B (MafB), B-cell lymphoma 6 (Bcl6), and interferon regulatory factor-8 (Irf8).
The revised WHO classification moved all aggressive B-cell lymphomas with a MYC translocation and a concurrent translocation of BCL2 and/or BCL6 into a single diagnostic category.
Here, we find that the B cell lymphoma 6 (BCL6) repressor is enriched in the fed state and converges genome-wide with PPARα to potently suppress the induction of fasting transcription.
Blocking B cell lymphoma 6 (BCL6; the master transcription factor for Tfh cells) represses HIV infection of tonsillar CD4<sup>+</sup> Tfh <i>ex vivo</i>, reduces GC formation, and limits immune activation <i>in vivo</i> We assessed the anti-HIV activity of a novel BCL6 inhibitor, FX1, in Tfh/non-Tfh CD4<sup>+</sup> T cells and its impact on T cell activation and SAMHD1 phosphorylation (Thr592).
Recently, high-grade B-cell lymphomas with MYC and BCL2 and/or BCL6 rearrangements have been categorized separately from diffuse large B-cell lymphoma or BL.
A t(3;8)(q27;q24) rarely occurs in B-cell lymphomas that results in a unique "pseudo-double-hit" BCL6-MYC fusion, indistinguishable by interphase fluorescence in situ hybridization (FISH) from more conventional DTHL with independent MYC and BCL6 translocations.
Quantitative real-time PCR and Western blotting were used to detect the expression levels of miR-192, C-X-C chemokine receptor type 5 (CXCR5), B-cell lymphoma 6 (BCL-6) and inducible T-cell costimulator (ICOS).
B cell lymphoma 6 (BCL6) is a transcriptional repressor critical for the development and maintenance of germinal centers (GCs), which are required for generation of an effective humoral immune response.
A fluorescent in situ hybridization panel for lymphoma showed rearrangement of Immunoglobulin heavy chain (IGH) and B-cell lymphoma 6 (BCL6), respectively, suggesting fusion of BCL6/IGH.