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)

XL TCL1 BA hybridized to lymphocytes. One aberrant interphase nucleus with one fusion signal, and one separate orange and green signal is shown, representing a rearrangement with involvement of the TCL1 gene cluster.

• 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

• Utility and performance of bacterial artificial chromosomes-on-beads assays in chromosome analysis of clinical prenatal samples, products of conception and blood samples.
• A child with multiple congenital anomalies due to partial trisomy 7q22.1 → qter resulting from a maternally inherited balanced translocation: a case report and review of literature.
• Distinct roles of ATM and ATR in the regulation of ARP8 phosphorylation to prevent chromosome translocations.
• Heterogeneous MYCN amplification in neuroblastoma: a SIOP Europe Neuroblastoma Study.
• Immense random colocalization, revealed by automated high content image cytometry, seriously questions FISH as gold standard for detecting EML4-ALK fusion.
• Fluorescence in situ hybridisation assays designed for del(7q) detection uncover more complex rearrangements in myeloid leukaemia cell lines
• Detection of t(7;12)(q36;p13) in paediatric leukaemia using dual colour fluorescence in situ hybridisation.
• A rare case of t(11;22) in a mantle cell lymphoma like B-cell neoplasiaresulting in a fusion of IGL and CCND1: case report.
• Genomic DNA-chip hybridization in t(11;14)-positive mantle cell lymphomas shows a high frequency of aberrations and allows a refined characterization of consensus regions.