1. Characterization of a pediatric T-cell acute lymphoblastic leukemia patient with simultaneous LYL1 and LMO2 rearrangements
- Author
-
Jessica G.C.A.M. Buijs-Gladdines, Maartje J. Vuerhard, Jules P.P. Meijerink, Irene Homminga, Anton W. Langerak, Rob Pieters, Pediatrics, and Immunology
- Subjects
Male ,LMO2 ,T cell ,Chromosomal translocation ,Biology ,Precursor T-Cell Lymphoblastic Leukemia-Lymphoma ,Translocation, Genetic ,LYL1 ,Proto-Oncogene Proteins ,hemic and lymphatic diseases ,Basic Helix-Loop-Helix Transcription Factors ,Tumor Cells, Cultured ,Homologous chromosome ,medicine ,Cluster Analysis ,Humans ,Child ,Gene ,Adaptor Proteins, Signal Transducing ,Oncogene ,Hematology ,LIM Domain Proteins ,Molecular biology ,Neoplasm Proteins ,medicine.anatomical_structure ,Cancer research ,Original Articles and Brief Reports ,TAL1 - Abstract
Translocation of the LYL1 oncogene are rare in T-cell acute lymphoblastic leukemia, whereas the homologous TAL1 gene is rearranged in approximately 20% of patients. Previous gene-expression studies have identified an immature T-cell acute lymphoblastic leukemia subgroup with high LYL1 expression in the absence of chromosomal aberrations. Molecular characterization of a t(7;19)(q34;p13) in a pediatric T-cell acute lymphoblastic leukemia patient led to the identification of a translocation between the TRB@ and LYL1 loci. Similar to incidental T-cell acute lymphoblastic leukemia cases with synergistic, double translocations affecting TAL1/2 and LMO1/2 oncogenes, this LYL1-translocated patient also had an LMO2 rearrangement pointing to oncogenic cooperation between LYL1 and LMO2. In hierarchical cluster analyses based on gene-expression data, this sample consistently clustered along with cases having TAL1 or LMO2 rearrangements. Therefore, LYL1-rearranged cases are not necessarily associated with immature T-cell development, despite high LYL1 levels, but elicit a TALLMO expression signature.
- Published
- 2011
- Full Text
- View/download PDF