Turcas Cristina, Moisoiu Vlad, Stefancu Andrei, Jurj Ancuta, Iancu Stefania D, Teodorescu Patric, Pasca Sergiu, Bojan Anca, Trifa Adrian, Iluta Sabina, Zimta Alina-Andreea, Petrushev Bobe, Zdrenghea Mihnea, Bumbea Horia, Coriu Daniel, Dima Delia, Leopold Nicolae, Tomuleasa Ciprian
Department of Hematology, Iuliu Hatieganu University of Medicine and Pharmacy, Cluj-Napoca, Romania.
Department of Hematology, "Ion Chiricuta" Institute of Oncology, Cluj-Napoca, Romania.
Front Oncol. 2020 Jun 29;10:1024. doi: 10.3389/fonc.2020.01024. eCollection 2020.
Acute promyelocytic leukemia (APL) is characterized by a unique chromosome translocation t(15;17)(q24;q21), which leads to the PML/RARA gene fusion formation. However, it is acknowledged that this rearrangement alone is not able to induce the whole leukemic phenotype. In addition, epigenetic processes, such as DNA methylation, may play a crucial role in leukemia pathogenesis. DNA methylation, catalyzed by DNA methyltransferases (DNMTs), involves the covalent transfer of a methyl group (-CH3) to the fifth carbon of the cytosine ring in the CpG dinucleotide and results in the formation of 5-methylcytosine (5-mC). The aberrant gene promoter methylation can be an alternative mechanism of tumor suppressor gene inactivation. Understanding cancer epigenetics and its pivotal role in oncogenesis, can offer us not only attractive targets for epigenetic treatment but can also provide powerful tools in monitoring the disease and estimating the prognosis. Several genes of interest, such as RARA, RARB, p15, p16, have been studied in APL and their methylation status was correlated with potential diagnostic and prognostic significance. In the present manuscript we comprehensively examine the current knowledge regarding DNA methylation in APL pathogenesis. We also discuss the perspectives of using the DNA methylation patterns as reliable biomarkers for measurable residual disease (MRD) monitoring and as a predictor of relapse. This work also highlights the possibility of detecting aberrant methylation profiles of circulating tumor DNA (ctDNA) through liquid biopsies, using the conventional methods, such as methylation-specific polymerase chain reaction (MS-PCR), sequencing methods, but also revolutionary methods, such as surface-enhanced Raman spectroscopy (SERS).
急性早幼粒细胞白血病(APL)的特征是独特的染色体易位t(15;17)(q24;q21),这导致PML/RARA基因融合形成。然而,人们认识到仅这种重排不足以诱导整个白血病表型。此外,表观遗传过程,如DNA甲基化,可能在白血病发病机制中起关键作用。DNA甲基化由DNA甲基转移酶(DNMTs)催化,涉及将甲基(-CH3)共价转移到CpG二核苷酸中胞嘧啶环的第五个碳原子上,导致形成5-甲基胞嘧啶(5-mC)。异常的基因启动子甲基化可能是肿瘤抑制基因失活的另一种机制。了解癌症表观遗传学及其在肿瘤发生中的关键作用,不仅可以为表观遗传治疗提供有吸引力的靶点,还可以为监测疾病和评估预后提供有力工具。在APL中已经研究了几个感兴趣的基因,如RARA、RARB、p15、p16,它们的甲基化状态与潜在的诊断和预后意义相关。在本手稿中,我们全面审视了关于APL发病机制中DNA甲基化的现有知识。我们还讨论了将DNA甲基化模式用作可测量残留疾病(MRD)监测的可靠生物标志物以及作为复发预测指标的前景。这项工作还强调了通过液体活检,使用常规方法,如甲基化特异性聚合酶链反应(MS-PCR)、测序方法,以及革命性方法,如表面增强拉曼光谱(SERS),检测循环肿瘤DNA(ctDNA)异常甲基化谱的可能性。