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B-cell CLL/lymphoma 7A

BCL7A, bcl7
This gene is directly involved, with Myc and IgH, in a three-way gene translocation in a Burkitt lymphoma cell line. As a result of the gene translocation, the N-terminal region of the gene product is disrupted, which is thought to be related to the pathogenesis of a subset of high-grade B cell non-Hodgkin lymphoma. The N-terminal segment involved in the translocation includes the region that shares a strong sequence similarity with those of BCL7B and BCL7C. Two transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: BCL7B, BCL7C, c-Myc, Barr, bcl-6
Papers on BCL7A
Genipin as a novel chemical activator of EBV lytic cycle.
Kang et al., Taegu, South Korea. In J Microbiol, Feb 2015
In SNU719 cells, one of EBVaGCs, genipin caused significant cytotoxicity (70 μM), induced methylation on EBV C promoter and tumor suppressor gene BCL7A, arrested cell-cycle progress (S phases), upregulated EBV latent/lytic genes in a dose-dependent manner, stimulated EBV progeny production, activated EBV F promoter for EBV lytic activation, and suppressed EBV infection.
The Tumor Suppressor BCL7B Functions in the Wnt Signaling Pathway.
Mitani et al., Tokyo, Japan. In Plos Genet, 2015
Human BCL7 gene family consists of BCL7A, BCL7B, and BCL7C.
Cordycepin is a novel chemical suppressor of Epstein-Barr virus replication.
Kang et al., Taegu, South Korea. In Oncoscience, 2013
Interestingly, cordycepin increased BCL7A methylation in SNU719 cells by up to 58% and decreased demethylation by up to 37%.
Identification of genes specifically methylated in Epstein-Barr virus-associated gastric carcinomas.
Sakaida et al., Ube, Japan. In Cancer Sci, 2013
To identify genes specifically methylated in EBV-associated gastric carcinomas (EBVaGC), we focused on seven genes, TP73, BLU, FSD1, BCL7A, MARK1, SCRN1, and NKX3.1, based on the results of methylated CpG island recovery on chip assay.
Proteomic and bioinformatic analysis of mammalian SWI/SNF complexes identifies extensive roles in human malignancy.
Crabtree et al., United States. In Nat Genet, 2013
To understand the full extent of their involvement, we conducted a proteomic analysis of endogenous mSWI/SNF complexes, which identified several new dedicated, stable subunits not found in yeast SWI/SNF complexes, including BCL7A, BCL7B and BCL7C, BCL11A and BCL11B, BRD9 and SS18.
Nonimmunoglobulin target loci of activation-induced cytidine deaminase (AID) share unique features with immunoglobulin genes.
Honjo et al., Kyoto, Japan. In Proc Natl Acad Sci U S A, 2012
Along with known AID targets, this screen identified a set of unique genes (SNHG3, MALAT1, BCL7A, and CUX1) and confirmed that these loci accumulated mutations as frequently as Ig locus after AID activation.
SS18 together with animal-specific factors defines human BAF-type SWI/SNF complexes.
Logie et al., Nijmegen, Netherlands. In Plos One, 2011
Furthermore, SS18L1, DPF1, DPF2, DPF3, BRD9, BCL7A, BCL7B and BCL7C were identified.
Identification of modifier genes for cutaneous malignant melanoma in melanoma-prone families with and without CDKN2A mutations.
Goldstein et al., Bethesda, United States. In Int J Cancer, 2010
Our analyses identified some candidate genes such as FAS, BCL7A, CASP14, TRAF6, WRN, IL9, IL10RB, TNFSF8, TNFRSF9 and JAK3 that were associated with CMM risk (p<0.01,
Risk of non-Hodgkin lymphoma associated with germline variation in genes that regulate the cell cycle, apoptosis, and lymphocyte development.
Hartge et al., Rockville, United States. In Cancer Epidemiol Biomarkers Prev, 2009
Variants in BCL7A were strongly related to diffuse large B-cell lymphoma.
Array-based comparative genomic hybridization in early-stage mycosis fungoides: recurrent deletion of tumor suppressor genes BCL7A, SMAC/DIABLO, and RHOF.
Amerio et al., Roma, Italy. In Genes Chromosomes Cancer, 2008
deletion of genes BCL7A in early-stage mycosis fungoides.
Genetic and phenotypic analysis of B-cell post-transplant lymphoproliferative disorders provides insights into disease biology.
Bhagat et al., New York City, United States. In Hematol Oncol, 2008
To gain better insights into PTLD pathogenesis, we characterized the phenotypes, immunoglobulin (Ig) gene alterations and non-Ig gene (BCL6, RhoH/TTF, c-MYC, PAX5, CIITA, BCL7A, PIM1) mutations of 21 PTLD, including an IM-like lesion, 8 P-PTLD and 12 M-PTLD.
Genomic deletions correlate with underexpression of novel candidate genes at six loci in pediatric pilocytic astrocytoma.
Warr et al., London, United Kingdom. In Neoplasia, 2008
Loss of four individual clones was also associated with reduced gene expression including SH3GL2 at 9p21.2-p23, BCL7A (which shares 90% sequence homology with BCL7B) at 12q24.33,
Using expression profiling data to identify human microRNA targets.
Morris et al., Toronto, Canada. In Nat Methods, 2007
We experimentally verified our predictions by investigating the result of let-7b downregulation in retinoblastoma using quantitative reverse transcriptase (RT)-PCR and microarray profiling: some of our verified let-7b targets include CDC25A and BCL7A.
Germinal center B cell-like (GCB) and activated B cell-like (ABC) type of diffuse large B cell lymphoma (DLBCL): analysis of molecular predictors, signatures, cell cycle state and patient survival.
Dandekar et al., Würzburg, Germany. In Cancer Inform, 2006
A key regulatory network, distinguishing marked over-expression in ABC from that in GCB, is built by: ASB13, BCL2, BCL6, BCL7A, CCND2, COL3A1, CTGF, FN1, FOXP1, IGHM, IRF4, LMO2, LRMP, MAPK10, MME, MYBL1, NEIL1 and SH3BP5.
Epigenetic profiling of cutaneous T-cell lymphoma: promoter hypermethylation of multiple tumor suppressor genes including BCL7a, PTPRG, and p73.
Tensen et al., Leiden, Netherlands. In J Clin Oncol, 2005
Promoter hypermethylation of BCL7a is associated with cutaneous T-cell lymphoma
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