MetaSystems Probes has received IVDR certification for our initial 26 fluorescence in situ hybridization (FISH) probes from the notified body, BSI. Achieving this milestone was not without its challenges, and we are delighted to have accomplished IVDR certification for this probe set at an early stage.
XL TCL1 BA
Break Apart Probe
- Order Number
- D-5142-100-OG
- Package Size
- 100 µl (10 Tests)
- Chromosome
- 1414
- Regulatory Status
- IVDD
IVDR Certification
This probe is IVDR-certified in compliance with the Regulation (EU) 2017/746 on in vitro diagnostic medical devices (IVDR).
MetaSystems Probes has already certified a large part of its portfolio, according to IVDR. For organizational reasons, we currently provide only the IVDD product.
XL TCL1 BA is designed as a break apart probe. The orange labeled probe hybridizes proximal to the TCL1A/TCL1B gene region at 14q32.1, the green labeled probe hybridizes distal to TCL1A/TCL1B.
Probe maps are created in accordance with the intended purpose of the product. Solid colored bars do not necessarily indicate that the probe fully covers the indicated genomic region. Therefore, caution is advised when interpreting results generated through off-label use. Probe map details based on UCSC Genome Browser GRCh37/hg19. Map components not to scale. Further information is available on request.
The gene TCL1A (TCL1 family AKT coactivator A, previously known as T-cell leukaemia/lymphoma 1A), has been described first in the early 1990s. It belongs to the TCL1 gene family including TCL1A (14q32.13), TCL1B (14q32.13) and MTCP1 (Xq28). Physiologically, the TCL1-encoded protein is expressed in fetal tissues and during early developmental stages of lymphocytes. It regulates many proteins responsible for cellular proliferation, survival and epigenetic modifications through multiple signalling pathways.
Dysregulated TCL1 expression levels have been detected in chronic lymphocytic leukaemia (CLL), various lymphomas and in T-cell prolymphocytic leukaemia (T-PLL). In T-cells, TCL1 dysregulation is caused by chromosomal rearrangement events bringing TCL1 under the control of T-cell receptor (TCR) enhancer elements. Two distinct breakpoint clusters have been described, which are located on both sides of a 160kb region flanking the TCL1A/TCL1B/TCL6 gene cluster. The rearrangements leading to TCL1A translocations with TCRα/TCRδ and TCRβ gene loci have been characterized precisely. The underlying chromosomal rearrangements are inv(14)(q11q32), being the most common aberration, t(14;14)(q11;q32.1) and t(7;14)(q35;q32.1). Phage display technology- and structure-based drug design approaches are used to target TCL1, due to its major role in the activation of different survival and proliferation maintaining pathways.
Clinical Applications
- T-Cell Prolymphocytic Leukemia (T-PLL)
Normal Cell:
Two green-orange colocalization/fusion signals (2GO).
Aberrant Cell (typical results):
One green-orange colocalization/fusion signal (1GO), one separate green (1G) and orange (1O) signal each resulting from a chromosome break in the respective locus.
- Virgilio et al (1994) PNAS 91: 12530- 12534
- Saitou et al (2000) Oncogene 19: 2796- 2802
- Paduano et al (2018) Front Oncol doi:10.3389/fonc.2018.00317