BAL is a novel risk-related gene in diffuse large B-cell lymphomas that enhances cellular migration

Blood. 2000 Dec 15;96(13):4328-34.


Clinical risk factor models such as the International Prognostic Index are used to identify diffuse large B-cell lymphoma (DLB-CL) patients with different risks of death from their diseases. To elucidate the molecular bases for these observed clinical differences in outcome, differential display was used to identify a novel gene, termed BAL (B-aggressive lymphoma), which is expressed at significantly higher levels in fatal high-risk DLB-CLs than in cured low-risk tumors. The major BAL complementary DNA encodes a previously uncharacterized 88-kd nuclear protein with a duplicated N-terminal domain homologous to the nonhistone portion of histone-macroH2A and a C-terminal alpha-helical region with 2 short coiled-coil domains. Of note, the BAL N-terminus and secondary structure resemble those of a recently identified human protein, KIAA1268. In addition, both BAL and KIAA1268 map to chromosome 3q21, further suggesting that these genes belong to a newly identified family. BAL is expressed at increased levels in DLB-CL cell lines with an activated peripheral B cell, rather than a germinal center B cell, phenotype. This observation and the characteristic dissemination of high risk DLB-CLs prompted studies regarding the role of BAL in B-cell migration. In classical transwell assays, stable BAL-overexpressing B-cell lymphoma transfectants had significantly higher rates of migration than vector-only transfectants, indicating that the risk-related BAL gene promotes malignant B-cell migration. (Blood. 2000;96:4328-4334)

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Amino Acid Sequence
  • B-Lymphocytes / drug effects
  • B-Lymphocytes / pathology*
  • Cell Movement / drug effects
  • Cell Movement / genetics*
  • Chemokine CXCL12
  • Chemokines, CXC / pharmacology
  • Cloning, Molecular
  • Gene Expression Regulation, Neoplastic
  • Genes*
  • Humans
  • In Situ Hybridization, Fluorescence
  • Lymphoma, Large B-Cell, Diffuse / genetics*
  • Lymphoma, Large B-Cell, Diffuse / pathology
  • Lymphoma, Non-Hodgkin / genetics
  • Lymphoma, Non-Hodgkin / pathology
  • Molecular Sequence Data
  • Neoplasm Proteins / genetics*
  • Neoplasm Proteins / physiology
  • Poly(ADP-ribose) Polymerases
  • Recombinant Fusion Proteins / physiology
  • Recombinant Proteins / pharmacology
  • Risk
  • Sequence Alignment
  • Sequence Homology, Amino Acid
  • Transfection
  • Tumor Cells, Cultured / drug effects
  • Tumor Cells, Cultured / pathology


  • CXCL12 protein, human
  • Chemokine CXCL12
  • Chemokines, CXC
  • Neoplasm Proteins
  • PARP9 protein, human
  • Recombinant Fusion Proteins
  • Recombinant Proteins
  • Poly(ADP-ribose) Polymerases