## Abstract T‐cell acute lymphoblastic leukemia (T‐ALL) is the result of multiple oncogenic insults of thymocytes. Recently, new __ABL1__ fusion genes have been identified that provide proliferation and survival advantage to lymphoblasts. These are the __NUP214‐ABL1__ fusion gene, on amplified epis
Various types of rearrangements target TLX3 locus in T-cell acute lymphoblastic leukemia
✍ Scribed by Xin Ying Su; Maryvonne Busson; Véronique Della Valle; Paola Ballerini; Nicole Dastugue; Pascaline Talmant; Adolfo A. Ferrando; Dominique Baudry-Bluteau; Serge Romana; Roland Berger; Olivier A. Bernard
- Publisher
- John Wiley and Sons
- Year
- 2004
- Tongue
- English
- Weight
- 141 KB
- Volume
- 41
- Category
- Article
- ISSN
- 1045-2257
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✦ Synopsis
Abstract
Most chromosomal translocations observed in T‐cell acute lymphoblastic leukemia (T‐ALL) often produce transcriptional activation of transcription factor oncogenes. Ectopic expression of the TLX3 (also known as HOX11L2) gene has been shown to be associated with a cryptic t(5;14)(q35;q32) translocation specific for a subtype of T‐ALL. Here we report several examples of variant and alternative translocations resulting in expression of TLX3 in T‐ALL, and we describe three of these translocations in detail. In particular, the CDK6 gene was rearranged in two t(5;7)(q35;q21) translocations. In two additional instances, fusion of the BCL11B (also known as CTIP2) and RANBP17/TLX3 loci were shown to result from subtle genomic insertion/deletion within these loci. This study further underscores that TLX3 expression in T‐ALL is strongly associated with the presence of genomic rearrangements. © 2004 Wiley‐Liss, Inc.
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