Overexpression of c-Maf contributes to T-cell lymphoma in both mice and human

Cancer Res. 2006 Jan 15;66(2):812-9. doi: 10.1158/0008-5472.CAN-05-2154.

Abstract

c-Maf translocation or overexpression has been observed in human multiple myeloma. Although c-maf might function as an oncogene in multiple myeloma, a role for this gene in other cancers has not been shown. In this study, we have found that mice transgenic for c-Maf whose expression was direct to the T-cell compartment developed T-cell lymphoma. Moreover, we showed that cyclin D2, integrin beta(7), and ARK5 were up-regulated in c-Maf transgenic lymphoma cells. Furthermore, 60% of human T-cell lymphomas (11 of 18 cases), classified as angioimmunoblastic T-cell lymphoma, were found to express c-Maf. These results suggest that c-Maf might cause a type of T-cell lymphoma in both mice and humans and that ARK5, in addition to cyclin D2 and integrin beta(7), might be downstream target genes of c-Maf leading to malignant transformation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Transformation, Neoplastic
  • Cyclin D2
  • Cyclins / biosynthesis
  • Gene Expression Profiling
  • Humans
  • Integrin beta Chains / biosynthesis
  • Lymphoma, T-Cell / genetics*
  • Lymphoma, T-Cell / physiopathology
  • Mice
  • Protein Kinases / biosynthesis
  • Proto-Oncogene Proteins c-maf / biosynthesis*
  • Proto-Oncogene Proteins c-maf / physiology
  • Repressor Proteins / biosynthesis
  • Up-Regulation

Substances

  • CCND2 protein, human
  • Ccnd2 protein, mouse
  • Cyclin D2
  • Cyclins
  • Integrin beta Chains
  • MAF protein, human
  • Maf protein, mouse
  • Proto-Oncogene Proteins c-maf
  • Repressor Proteins
  • integrin beta7
  • Protein Kinases
  • NUAK1 protein, human