Dysregulation of normal transcription is a feature of all acute leukaemias. In T-cell neoplasms, this is brought about by altered expression of normal transcription factor proteins, often as a consequence of chromosomal translocations or inversions placing these genes into close proximity of the promoter and enhancer elements of the T-cell receptor genes, TRA@ (TCRA), TRB@ (TCRB), TRG@ (TCRG) and TRD@ (TCRD)1.
Murine studies show that expression of mouse homologues of TLX1 (T-Cell Leukaemia Homeobox 1 or HOX11) can immortalize haematopoietic cells in vitro as the first of a potential two-hit mechanism leading to full malignancy2. This work suggests that TLX1, which is aberrantly expressed in 30% of adult and 5-10% of childhood T-ALL cases3, is an oncogene that can become dysregulated through the translocations t(10;14)(q24;q11) and t(7;10)(q35;q24), placing it into close proximity to TCRA/D and TCRB elements respectively4. Breakpoints are clustered within a region 10kb centromeric to and immediately adjacent to TLX1.
1. Korsmeyer SJ, Annual Rev Immunol 1992;10:785-807
2. Hawley RG et al., Oncogene 1994;9:1-12
3. Riz et al., Oncogene (2005) 24, 5561–5575
4. Dubé ID et al., Blood 1991;78(11):2996-3003
- Area of Interest*
This product is intended to be used on Carnoy’s solution (3:1 methanol/acetic acid) fixed haematological samples.
*Disease information supported by the literature and is not a reflection of the intended purpose of this product.