Bcl10 is involved in t(1;14)(p22;q32) of MALT B cell lymphoma and mutated in multiple tumor types

Cell. 1999 Jan 8;96(1):35-45. doi: 10.1016/s0092-8674(00)80957-5.


MALT B cell lymphomas with t(1;14)(p22;q32) showed a recurrent breakpoint upstream of the promoter of a novel gene, Bcl10. Bcl10 is a cellular homolog of the equine herpesvirus-2 E10 gene: both contain an amino-terminal caspase recruitment domain (CARD) homologous to that found in several apoptotic molecules. Bcl10 and E10 activated NF-kappaB but caused apoptosis of 293 cells. Bcl10 expressed in a MALT lymphoma exhibited a frameshift mutation resulting in truncation distal to the CARD. Truncated Bcl10 activated NF-kappaB but did not induce apoptosis. Wild-type Bcl10 suppressed transformation, whereas mutant forms had lost this activity and displayed gain-of-function transforming activity. Similar mutations were detected in other tumor types, indicating that Bcl10 may be commonly involved in the pathogenesis of human malignancy.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adaptor Proteins, Signal Transducing*
  • Amino Acid Sequence
  • Animals
  • Apoptosis
  • B-Cell CLL-Lymphoma 10 Protein
  • Base Sequence
  • COS Cells
  • Cell Line, Transformed
  • Cell Transformation, Neoplastic
  • Chromosomes, Human, Pair 1*
  • Chromosomes, Human, Pair 14*
  • Cloning, Molecular
  • Gene Expression
  • HeLa Cells
  • Humans
  • Lymphoma, B-Cell, Marginal Zone / genetics*
  • Mice
  • Molecular Sequence Data
  • Mutation*
  • NF-kappa B / metabolism
  • Neoplasm Proteins / genetics*
  • Neoplasm Proteins / physiology
  • Neoplasms / genetics
  • Sequence Homology, Amino Acid
  • Translocation, Genetic*


  • Adaptor Proteins, Signal Transducing
  • B-Cell CLL-Lymphoma 10 Protein
  • BCL10 protein, human
  • Bcl10 protein, mouse
  • NF-kappa B
  • Neoplasm Proteins

Associated data

  • GENBANK/AJ006288
  • GENBANK/AJ006289
  • GENBANK/AJ006290
  • GENBANK/AJ006410