**4. Chromosomal and molecular abnormalities associated with ALL-T**

T-cell acute lymphoblastic leukemia (T-ALL) is a leukemia that develops when there is an accumulation of genomic lesions that impair T-cell growth. T-ALL is correlated with a lot of genetic diversity. The accumulation of a variety of genetic and epigenetic defects leads to leukemic transformation [61]. As a result of excessive neoplastic cell proliferation, they cause disorders of cell differentiation, apoptosis, oncogene activation, and suppressor inhibition. The first genetic abnormalities in T-ALL patients were chromosome aberrations. Except for tetraploidy, which occurs in around 5% of cases, numerical changes are uncommon and have little prognostic significance.

The identification of chromosomal anomalies, such as 9p deletions that result in CDKN2A (p16) and CDKN2B (p15) inactivation, and translocations affecting T-cell receptor genes, has been crucial in gaining an understanding of the genetic defects present in T-ALL.

The proportion of cytogenetically normal cases at diagnosis is higher in T-ALL than in B-ALL, with about 50 percent of patients with T-ALL possessing a normal karyotype. Approximately one-third of T-ALL patients have a translocation involving one of the T-cell receptor genes (TCR), with a breakpoint at 14q11 (*TCRA/ TCRD*) or 7q34 (*TCRB*), juxtaposing the T-cell receptor genes to pivotal transcription factor genes, such as TAL1, TAL2, LYL1, OLIG2, LMO1, LMO2, TLX1 (HOX11), TLX3 (HOX11L2), NKX2–1, NKX2–2, NKX2–5, HOXA genes, MYC, and MYB. In the adult population, the translocation t(10;14)(q24;q11.2), which results in overexpression of the *TLX1 (HOX11)* gene, is the most common and is associated with a favorable outcome [62, 63]. In addition, T-ALLs can contain cryptic rearrangements of ABL1 that may be amenable to TKI therapy. In general, studies of gene expression profiling have helped to classify T-ALL into molecular subgroups characterized by distinct signatures of gene expression and aberrant activation of specific oncogenes of the T-ALL transcription factor, including MEF2C, HOXA, TLX1, NKX2.1, TLX3, TAL1, LMO1, and LMO2 [41, 64].
