Hematology and Bone Marrow Transplantation Unit, Department of Medicine, Molecular Medicine Laboratory, University of Perugia, Perugia, Italy.
Hematology and Bone Marrow Transplantation Unit, Department of Medicine, Molecular Medicine Laboratory, University of Perugia, Perugia, Italy.
J Mol Diagn. 2020 May;22(5):629-639. doi: 10.1016/j.jmoldx.2020.02.004. Epub 2020 Mar 4.
T-cell acute lymphoblastic leukemia (T-ALL) results from deregulation of a number of genes via multiple genomic mechanisms. We designed a comprehensive fluorescence in situ hybridization (CI-FISH) assay that consists of genomic probes to simultaneously investigate oncogenes and oncosuppressors recurrently involved in chromosome rearrangements in T-ALL, which was applied to 338 T-ALL cases. CI-FISH provided genetic classification into one of the well-defined genetic subgroups (ie, TAL/LMO, HOXA, TLX3, TLX1, NKX2-1/2-2, or MEF2C) in 80% of cases. Two patients with translocations of the LMO3 transcription factor were identified, suggesting that LMO3 activation may serve as an alternative to LMO1/LMO2 activation in the pathogenesis of this disease. Moreover, intrachromosomal rearrangements that involved the 10q24 locus were found as a new mechanism of TLX1 activation. An unequal distribution of cooperating genetic defects was found among the six genetic subgroups. Interestingly, deletions that targeted TCF7 or TP53 were exclusively found in HOXA T-ALL, LEF1 defects were prevalent in NKX2-1 rearranged patients, CASP8AP2 and PTEN alterations were significantly enriched in TAL/LMO leukemias, and PTPN2 and NUP214-ABL1 abnormalities occurred in TLX1/TLX3. This work convincingly shows that CI-FISH is a powerful tool to define genetic heterogeneity of T-ALL, which may be applied as a rapid and accurate diagnostic test.
T 细胞急性淋巴细胞白血病(T-ALL)是由于多个基因组机制导致多个基因失调引起的。我们设计了一种全面的荧光原位杂交(CI-FISH)检测方法,该方法包含基因组探针,可同时研究涉及 T-ALL 染色体重排的常见癌基因和肿瘤抑制基因,该方法应用于 338 例 T-ALL 病例。CI-FISH 可将 80%的病例进行明确的遗传分类,归入以下明确的遗传亚组之一(即 TAL/LMO、HOXA、TLX3、TLX1、NKX2-1/2-2 或 MEF2C)。发现了 2 例 LMO3 转录因子易位的患者,表明 LMO3 激活可能替代 LMO1/LMO2 激活,成为该疾病发病机制的一种替代机制。此外,还发现了涉及 10q24 位的染色体内重排,这是 TLX1 激活的一种新机制。在这六个遗传亚组中发现了具有合作性遗传缺陷的非均等分布。有趣的是,靶向 TCF7 或 TP53 的缺失仅在 HOXA T-ALL 中发现,LEF1 缺陷在 NKX2-1 重排患者中常见,CASP8AP2 和 PTEN 改变在 TAL/LMO 白血病中明显富集,而 PTPN2 和 NUP214-ABL1 异常发生在 TLX1/TLX3 中。这项工作令人信服地表明,CI-FISH 是定义 T-ALL 遗传异质性的有力工具,可作为一种快速而准确的诊断检测方法。