HOX11L2/TLX3 is transcriptionally activated through T-cell regulatory elements downstream of BCL11B as a result of the t(5;14)(q35;q32)

Blood. 2006 Dec 15;108(13):4198-201. doi: 10.1182/blood-2006-07-032953. Epub 2006 Aug 22.

Abstract

The t(5;14)(q35;q32) chromosomal translocation is specifically observed in up to 20% of childhood T-cell acute lymphoblastic leukemia (T-ALL). It affects the BCL11B/CTIP2 locus on chromosome 14 and the RANBP17-TLX3/HOX11L2 region on chromosome 5. It leads to ectopic activation of TLX3/HOX11L2. To investigate the reasons of the association between t(5;14) and T-ALL, we isolated the translocation breakpoints in 8 t(5;14) patients. Sequence analyses did not involve recombinase activity in the genesis of the translocation. We used DNAse1 hypersensitive experiments to locate transcriptional regulatory elements downstream of BCL11B. By transient transfection experiments, 2 of the 6 regions demonstrated cis-activation properties in T cells and were also effective on the TLX3 promoter. Our data indicate that the basis of the specific association between t(5;14) and T-ALL lies on the juxtaposition of TLX3 to long-range cis-activating regions active during T-cell differentiation.

Publication types

  • Clinical Trial
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Differentiation / genetics
  • Chromosomes, Human, Pair 14 / genetics*
  • Chromosomes, Human, Pair 5 / genetics*
  • DNA-Binding Proteins / biosynthesis
  • DNA-Binding Proteins / genetics*
  • Homeodomain Proteins / biosynthesis
  • Homeodomain Proteins / genetics*
  • Humans
  • Jurkat Cells
  • Leukemia-Lymphoma, Adult T-Cell / genetics*
  • Leukemia-Lymphoma, Adult T-Cell / metabolism
  • Leukemia-Lymphoma, Adult T-Cell / pathology
  • Oncogene Proteins / biosynthesis
  • Oncogene Proteins / genetics*
  • Oncogene Proteins, Fusion / biosynthesis
  • Oncogene Proteins, Fusion / genetics*
  • Promoter Regions, Genetic / genetics
  • Repressor Proteins / biosynthesis
  • Repressor Proteins / genetics*
  • T-Lymphocytes / metabolism
  • T-Lymphocytes / pathology
  • Transcription, Genetic
  • Translocation, Genetic*
  • Tumor Suppressor Proteins / biosynthesis
  • Tumor Suppressor Proteins / genetics*

Substances

  • BCL11B protein, human
  • DNA-Binding Proteins
  • Homeodomain Proteins
  • Oncogene Proteins
  • Oncogene Proteins, Fusion
  • Repressor Proteins
  • TLX3 protein, human
  • Tumor Suppressor Proteins