Disease relevance of BCL9

• Fusion of the BCL9 HD2 domain to E1A increases the cytopathic effect of an oncolytic adenovirus that targets colon cancer cells [1].
• Recently, BCL9 has been cloned from a pre-B-cell lymphoblastic leukemia cell line, which carried a t(1:14)(q21;q32) [2].
• We describe a 17-year-old female who developed B-cell lymphoma 9 years following the occurrence of donor-origin acute myeloid leukemia in her brother for whom she had donated marrow [3].

High impact information on BCL9

• Stimulation of the Wnt pathway leads to the association of beta-catenin with Tcf and BCL9 in the nucleus, resulting in the transactivation of Wnt target genes [4].
• Crystal Structure of a beta-Catenin/BCL9/Tcf4 Complex [4].
• Low-level expression of BCL9 was detected in Epstein-Barr virus-transformed normal B cells by Northern blot; in contrast, abundant BCL9 expression was observed in CEMO-1, indicating that deregulated expression of this gene was one pathological consequence of the translocation [5].
• Molecular cloning of translocation t(1;14)(q21;q32) defines a novel gene (BCL9) at chromosome 1q21 [5].
• Full-length BCL9 cDNA clones were obtained from a normal human fetal brain cDNA library supplemented by 5' and 3' RACE [5].

Biological context of BCL9

• Candidate oncogenes bordering this interval (BCL9 and AF1Q) were not rearranged in any patient except one (AF1Q) [6].

Anatomical context of BCL9

• These data suggest that BCL9 may be the target of translocation in some B-cell malignancies with abnormalities of 1q21 and that deregulated BCL9 expression may be important in their pathogenesis [5].
• In addition, the BCL9 gene was not over-expressed in SKI-DLCL-1 cell line [2].

Other interactions of BCL9

• To characterize this instability further, we performed spectral karyotyping and fluorescence in situ hybridization with probes for satII/III (1q12), BCL9 (1q21), and IL6R (1q21) on the karyotypes of 44 patients with known 1q aberrations [7].

Analytical, diagnostic and therapeutic context of BCL9

• Screening of a panel of 39 B-cell malignancies with 1q abnormalities by Southern blot showed one additional case with a breakpoint in the 3' UTR of BCL9, indicating that this was a recurrent breakpoint [5].

References