Abstract
Abstract
Background: The primary tumours-specific TAL1 and TAL2 genes translocate to T-ALL. Precisely, the TAL2 (T-cell acute lymphocytic leukaemia 2) gene translocates to the chromosome breakpoint of t (7; 9) associated with the T-cell. The TAL2 genes transform in the TCR beta-chain identified in chromosome 7. TAL1 and TAL2 correspond to the LYL1 gene and represent a unique subgroup of bHLH TFs mediators of T-cell leukaemogenesis. Also, the magnitude of a subgroup of bHLH TFs (TAL1/TAL2 and LYL1) genes conserve in evolution. Those nuclear transcription factor genes control the malignant growth of lymphocytes.
Objective: The study aimed to investigate a subgroup of bHLH TFs of TAL1, TAL2, and LYL1 genes in the mammalian genomes. An analysis of the T-ALL-associated genes is mandatory to explore the molecular mechanisms involved in chromosomal breakpoint and translocation in particular organisms.
Methods: Analysis data summarized the number of TAL1, TAL1, and LYL1 genes and particular bHLH domains in the two different genomes. Observation data suggested the tumour-specific translocation of the TAL1, TAL2, and LYL1 genes in humans. Also, the conserved domain, motifs, phylogeny, gene expression, chromosome location and gene network analysis documented a subgroup of bHLH transcription factor genes associated with T-ALL.
Conclusions: The wealth of new reports supported unique genetic and phenotypic attributes of T-cell-leukaemogenesis. Some advanced reports and new approaches also promote conventional wisdom. So, this study concluded a subgroup of bHLH transcription factor genes linked with the progress of T-cell leukaemogenesis.
Publisher
Research Square Platform LLC