Written | 2012-12 | Jean-Loup Huret |
Genetics, Dept Medical Information, University of Poitiers, CHU Poitiers Hospital, F-86021 Poitiers, France |
This article is an update of : |
2007-02 | Stevan Knezevich | |
BC Cancer Research Centre (BCCRC), Vancouver, British Columbia, Canada |
1998-09 | Jean-Pierre Kerckaert | |
Unite 124 INSERM, Institut de Recherches sur le Cancer, Place de Verdun, 59045 Lille cedex, France |
Identity |
Alias (NCBI) | BCL5 | LAZ3 | ZBTB27 | ZNF51 | BCL6A |
HGNC (Hugo) | BCL6 |
HGNC Alias symb | ZBTB27 | LAZ3 | BCL5 | BCL6A |
HGNC Previous name | ZNF51 |
HGNC Previous name | "zinc finger protein 51 | B cell CLL/lymphoma 6 | BCL6, transcription repressor" |
LocusID (NCBI) | 604 |
Atlas_Id | 20 |
Location | 3q27.3 [Link to chromosome band 3q27] |
Location_base_pair | Starts at 187721381 and ends at 187745468 bp from pter ( according to GRCh38/hg38-Dec_2013) [Mapping BCL6.png] |
Local_order | Gene orientation: telomere - 5' BCL6 3' - centromere. |
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BCL6 (3q27) - Courtesy Mariano Rocchi, Resources for Molecular Cytogenetics. | |
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BCL6 (B-Cell Lymphoma 6) Hybridization with Vysis break apart probe (Abbott Molecular, US) showing BCL6 on 3q27.3 (red-green or a fused yellow signal) - Courtesy Adriana Zamecnikova. | |
Fusion genes (updated 2017) | Data from Atlas, Mitelman, Cosmic Fusion, Fusion Cancer, TCGA fusion databases with official HUGO symbols (see references in chromosomal bands) |
ARID4B (1q42.3) / BCL6 (3q27.3) | BCL6 (3q27.3) / ADGRL2 (1p31.1) | BCL6 (3q27.3) / AFDN (6q27) | |
BCL6 (3q27.3) / BCL2 (18q21.33) | BCL6 (3q27.3) / BCL6 (3q27.3) | BCL6 (3q27.3) / C3 (19p13.3) | |
BCL6 (3q27.3) / CIITA (16p13.13) | BCL6 (3q27.3) / EIF4A2 (3q27.3) | BCL6 (3q27.3) / FBXO18 (10p15.1) | |
BCL6 (3q27.3) / HIST1H4I (6p22.1) | BCL6 (3q27.3) / HSP90AA1 (14q32.31) | BCL6 (3q27.3) / HSP90AB1 (6p21.1) | |
BCL6 (3q27.3) / IKZF1 (7p12.2) | BCL6 (3q27.3) / IL21R (16p12.1) | BCL6 (3q27.3) / KCNN4 (19q13.31) | |
BCL6 (3q27.3) / LCP1 (13q14.13) | BCL6 (3q27.3) / LONP1 (19p13.3) | BCL6 (3q27.3) / MBNL1 (3q25.1) | |
BCL6 (3q27.3) / MYBL1 (8q13.1) | BCL6 (3q27.3) / MYC (8q24.21) | BCL6 (3q27.3) / NACA (12q13.3) | |
BCL6 (3q27.3) / PIM1 (6p21.2) | BCL6 (3q27.3) / POU2AF1 (11q23.1) | BCL6 (3q27.3) / RAF1 (3p25.2) | |
BCL6 (3q27.3) / RHOH (4p14) | BCL6 (3q27.3) / SRSF3 (6p21.31) | BCL6 (3q27.3) / TFRC (3q29) | |
BCL6 (3q27.3) / TOX4 (14q11.2) | BCL6 (3q27.3) / TRBV20OR9-2 (-) | CIITA (16p13.13) / BCL6 (3q27.3) | |
DMRT1 (9p24.3) / BCL6 (3q27.3) | EIF4A2 (3q27.3) / BCL6 (3q27.3) | FSTL3 (19p13.3) / BCL6 (3q27.3) | |
GAPDH (12p13.31) / BCL6 (3q27.3) | GAS5 (1q25.1) / BCL6 (3q27.3) | GRHPR (9p13.2) / BCL6 (3q27.3) | |
HIST1H4F (6p22.2) / BCL6 (3q27.3) | HIST1H4I (6p22.1) / BCL6 (3q27.3) | HRH4 (18q11.2) / BCL6 (3q27.3) | |
HSP90AA1 (14q32.31) / BCL6 (3q27.3) | HSP90AA2P (11p14.1) / BCL6 (3q27.3) | HSP90AB1 (6p21.1) / BCL6 (3q27.3) | |
IKZF1 (7p12.2) / BCL6 (3q27.3) | IL21R (16p12.1) / BCL6 (3q27.3) | JCHAIN (4q13.3) / BCL6 (3q27.3) | |
KCNN4 (19q13.31) / BCL6 (3q27.3) | LCP1 (13q14.13) / BCL6 (3q27.3) | LONP1 (19p13.3) / BCL6 (3q27.3) | |
LPP (3q28) / BCL6 (3q27.3) | LRMP (12p12.1) / BCL6 (3q27.3) | MBNL1 (3q25.1) / BCL6 (3q27.3) | |
MN1 (22q12.1) / BCL6 (3q27.3) | MYC (8q24.21) / BCL6 (3q27.3) | NACA (12q13.3) / BCL6 (3q27.3) | |
NAPA (19q13.32) / BCL6 (3q27.3) | PIM1 (6p21.2) / BCL6 (3q27.3) | POU2AF1 (11q23.1) / BCL6 (3q27.3) | |
RHOH (4p14) / BCL6 (3q27.3) | SAA2-SAA4 (11p15.1) / BCL6 (3q27.3) | SNHG5 (6q14.3) / BCL6 (3q27.3) | |
SRSF3 (6p21.31) / BCL6 (3q27.3) | ST6GAL1 (3q27.3) / BCL6 (3q27.3) | STAT5A (17q21.2) / BCL6 (3q27.3) | |
STPG1 (1p36.11) / BCL6 (3q27.3) | TFRC (3q29) / BCL6 (3q27.3) | TOX4 (14q11.2) / BCL6 (3q27.3) | |
DNA/RNA |
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Description | The gene is encoded by 11 exons that are located on chromosome 3q27 and is 24,3 kb. The 5' portion encodes for the BTB/POZ domain (broad-complex/tramtrack/bric-a-brac/pox virus/zinc finger), while the 3' end encodes for 6 DNA binding zinc fingers. The first ATG occurs in exon 3. |
Transcription | 3,8 kb mRNA. |
Protein |
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Description | The protein product is 706 amino acids with an estimated molecular weight of 78,8 kDa. |
Expression | Normally expressed in germinal center B and T cells, other lymphoid tissues, in skeletal muscle cells and in keratinocytes. Normally expressed in germinal center B and T cells, other lymphoid tissues, in skeletal muscle cells and in keratinocytes. |
Localisation | Nuclear paraspeckles/dots. |
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Function | Protein domains and functions The protein can bind to sequence specific DNA and repress its transcription in addition to recruiting other protein repressors. The DNA binding is mediated through the consensus sequence TTCCT(A/C)GAA (see below), while the protein-protein interactions are mediated through the BTB/POZ domain and it has been shown to interact with other zinc finger proteins and corepressors (including Histone Deacetylase 1 (HDAC1) and NCOR2 (Silencing Mediator of Retinoid and Thryoid Receptor 1 (SMRT1))). The carboxy terminus, on the other hand, is responsible for sequence specific DNA binding through its 6 zinc fingers. Consensus DNA motifs recognized by BCL6 BCL6 cellular function BCL6 repression activity BCL6 targets BCL6 regulation |
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Homology | BTB/POZ - Zinc Finger proteins (PLZF, HIC1, KUP, BAZF, ttk (drosophila), BrC (drosophila)...). |
Mutations |
Note | Chromosomal translocations involving BCL6 are found in 40% of diffuse large B-cell lymphomas (DLBCL), 5-10% of follicular lymphomas (FL), and 50% of nodular lymphocyte predominant Hodgkin lymphomas. Mutations in the autoregulatory region of BCL6 leads to a constitutive BCL6 expression (Pasqualucci et al., 2003). IRF4 response elements in the BCL6 gene mediate repression of BCL6. Mutations in the IRF4 repression region of BCL6 gene also leads to constitutive expression of BCL6 (Saito et al., 2007). MYC, BCL2, and BCL6 rearrangements were detected in 6%, 15%, and 29% respectively of diffuse large B-cell lymphoma (DLBCL) patients. Double or triple rearrangements were detected in 3% of these patients. MYC rearrangement was associated with a significantly worse overall survival. BCL6 rearrangement also predicted a significantly shorter overall survival, especially for the non-GC phenotype (Akyurek et al., 2012). |
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Implicated in |
Note | |
Entity | 3q27 rearrangements /NHL (non Hodgkin lymphomas) |
Disease | B cell non-Hodgkin Lymphoma (B-NHL) |
Prognosis | Generally considered to be a better prognosis if there is increased expression of BCL6. The mechanism by which its expression is increased does not seem to matter (ie different translocation partners increasing its expression results in the same prognosis). |
Cytogenetics | 3q27 rearrangements/aberrations are diverse and include: translocations, micro-deletions, point mutations and hypermutation. Approximately 50% of 3q27 translocations involves Ig genes at 14q32 (IgH), 2p12 (IgK) and 22q12 (IgL) (e.g. t(3;14)(q27;q32)). Less than half (~40%) include a variety of other chromosomal regions (1q21, 2q21, 4p11, 5q31, 6p21, 7p12, 8q24, 9p13, 11q13, 11q23, 12q11, 13q14-21, 14q11, 15q21; 16p11...). In addition, there are frequent bi-allelic alterations (translocation and deletion or mutation on the non-translocated allele). |
Hybrid/Mutated Gene | hybrid gene and transcripts are formed following promoter substitution between BCL6 and its different partners. Chimeric transcripts are generally detected containing the 5' part of the gene partner fused to the normal BCL6 exon 2 splice acceptor site. In some cases reciprocal chimeric transcripts driven by the 5' regulatory region of BCL6 fused to the partner gene coding region, have been characterised. - t(1;3)(q25;q27) the gene in 1q25 is GAS5 - t(2;3)(p12;q27) the gene in 2p12 is IGK - t(3;3)(q25;q27) the gene in 3q25 is MBNL1 - t(3;3)(q27;q27) the gene in 3q27 is ST6GAL1 - t(3;3)(q27;q27) the gene in 3q27 is EIF4A2 - t(3;3)(q27;q29) the gene in 3q29 is TFRC - t(3;4)(q27;p13) the gene in 4p13 is RHOH - t(3;6)(q27;p22) the gene in 6p22 is HIST1H4I - t(3;6)(q27;p21) the gene in 6p21 is PIM1 - t(3;6)(q27;p21) the gene in 6p21 is SFRS3 - t(3;6)(q27;q15) the gene in 6q15 is SNHG5 - t(3;7)(q27;p12) the gene in 7p12 is IKZF1 - t(3;7)(q27;q32) the gene in 7q32 is FRA7H - t(3;8)(q27;q24.1) the gene in 8q24.1 is MYC - t(3;9)(q27;p24) the gene in 9p24 is DMRT1 - t(3;9)(q27;p11) the gene in 9p11 is GRHPR - t(3;11)(q27;q23) the gene in 11q23 is POU2AF1 - t(3;12)(q27;p13) the gene in 12p13 is GAPDH - t(3;12)(q27;q12) the gene in 12q12 is LRMP - t(3;13)(q27;q14) the gene in 13q14 is LCP1 - t(3;14)(q27;q32) the gene in 14q32 is IGH - t(3;14)(q27;q32) the gene in 14q32 is HSP90AA1 - t(3;16)(q27;p13) the gene in 16p13 is CIITA - t(3;16)(q27;p11) the gene in 16p11 is IL21R - t(3;19)(q27;q13) the gene in 19q13 is NAPA - t(3;22)(q27;q11) the gene in 22q11 is IGL |
Abnormal Protein | No fusion protein. |
Entity | t(9;22)(q34;q11) leukemias |
Disease | BCL6 enables Ph+ acute lymphoblastic leukaemia cells to survive BCR-ABL1 kinase inhibition (Duy et al. 2011). In chronic myelogenous leukemia (CML), BCL6 acts as a critical effector downstream of FoxO in self-renewal signaling of CML-initiating cells. Therefore, pharmacological inhibition of BCL6 may represent a novel strategy to eradicate leukemia-initiating cells in CML (Hurtz et al., 2011). |
Entity | Breast cancer |
Disease | BCL6 protein is elevated in human breast cancers, especially in high-grade, poorly differentiated and metastatic breast cancer cases (Bos et al., 2003; Logarajah et al., 2003; Brill et al., 2010). PRL (prolactin) rapidly suppressed BCL6. Loss of PRL-STAT5a signaling and concomitant upregulation of BCL6 may represent a regulatory switch facilitating undifferentiated histology and poor prognosis (Brill et al., 2010). |
Entity | Bladder transitional cell carcinoma |
Disease | BCL6 protein overexpression is observed in half of the cases of transitional cell carcinoma. However, BCL6 over-expression has a negative correlation with the histological grade (Cho et al., 2007). |
Entity | Soft tissue tumors |
Disease | BCL6 expression is more frequent in malignant compared with benign/uncertain solitary fibrous tumors, as well as in leiomyosarcomas compared with leiomyomas (Walters et al., 2011). |
Entity | Neuroblastoma |
Disease | In the neuroblastic phenotype of neuroblastoma, BCL6 expression is associated with increased time to relapse and increased overall survival (Chamdin et al., 2009). |
Entity | Gastric cancer |
Disease | In a study of 100 gastric cancer cases, BCL6 was highly expressed in differentiated cancers and reduced or absent in undifferentiated cancers. However, survival was identical in BCL6-positive and BCL6-negative cases (Hirata et al., 2009). |
Entity | Multiple myeloma |
Disease | IL6 induces transcriptional up-regulation of BCL6 via JAK/STAT3 pathway. TNF (TNF alpha) up-regulates BCL6. BCL6 expression is mediated independantly via both JAK/STAT3 and NF-KB pathways in multiple myeloma cells (Hideshima et al., 2010). |
Breakpoints |
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Note | Clustered in a 3,3 kb EcoRI fragment (MTC) includind exon 1A and intron 1. |
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Citation |
This paper should be referenced as such : |
Huret, JL |
BCL6 (B-Cell Lymphoma 6) |
Atlas Genet Cytogenet Oncol Haematol. 2013;17(6):371-379. |
Free journal version : [ pdf ] [ DOI ] |
History of this paper: |
Kerkaert, JP. LAZ3 (lymphoma associated zinc finger on chromosome 3). Atlas Genet Cytogenet Oncol Haematol. 1999;3(1):4-5. |
http://documents.irevues.inist.fr/bitstream/handle/2042/37472/09-1998-BCL6ID20.pdf |
Knezevich, S. BCL6 (B-Cell Lymphoma 6). Atlas Genet Cytogenet Oncol Haematol. 2007;11(3):177-179. |
http://documents.irevues.inist.fr/bitstream/handle/2042/38432/02-2007-BCL6ID20.pdf |
Other Leukemias implicated (Data extracted from papers in the Atlas) [ 64 ] |
Other Solid tumors implicated (Data extracted from papers in the Atlas) [ 3 ] |
Soft tissues and Bone: Sarcoma with inv(X)(p11.4p11.22) BCOR/CCNB3
Head and Neck: Oral squamous cell carcinoma t(3;3)(p25;q27) BCL6/RAF1 |
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