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)1,2.
In T-PLL (a form of mature T-cell proliferation in patients with Ataxia Telangiectasia (AT)3), the (T-cell Leukaemia 1A/1B) gene cluster on chromosome 14q32 has been shown to be involved in a number of different chromosomal rearrangements, including the t(14;14)(q11;q32) and inv(14)(q11;q32), which bring elements of the cluster into close juxtaposition to, and under the control of, the TCR gene promoters and enhancers. There are two breakpoint regions in the gene cluster, each of which are observed in different neoplasms, though both are involved in either the inv(14) or t(14;14). Breakpoints are concentrated in regions centromeric and telomeric to the TCL1A, TCL6 and TCL1B genes4.
1. Korsmeyer SJ, Annual Rev Immunol 1992;10:785-807
2. Virgilio et al., PNAS 1994;91:12530-12534
3. Brito-Babpulle V, Catovsky D, Cancer Genet Cytogenet 1991;55:1-9
4. Saitou et al., Oncogene 2000;19:2796-802
- 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.