Kojima Kensuke, Tsuge Noriko, Yoshida Shohei, Umebara Dai, Nishida Yoshie, Miyazaki Shiori, Asagiri Tadashi
Department of Hematology, Kochi Medical School, Kochi University, Nankoku, Kochi, 783-8505, Japan.
Clinical Laboratory Department, Kochi Medical School Hospital, Kochi, Japan.
Int J Hematol. 2025 Sep 26. doi: 10.1007/s12185-025-04076-z.
Unbalanced whole-arm translocation der(5;19)(p10;q10) is a rare but recurrent cytogenetic aberration noted in patients with myelodysplastic neoplasms (MDS) and acute myeloid leukemia (AML). Eight cases of MDS/AML with der(5;19)(p10;q10) have been previously reported. Here, we describe three additional cases of MDS with der(5;19)(p10;q10) at our institution, in which we identified myeloid malignancy-associated mutations using next-generation sequencing. All patients had two TP53 mutations, each with >10% variant allele frequency, suggesting double-hit TP53 mutations. Double-hit TP53 mutations are only found in approximately 2% of patients with MDS, and may be involved in the development of the cytogenetic abnormalities der(5;19)(p10;q10), +19, and complex karyotype, often associated with exposure to alkylating agents. We propose der(5;19)(p10;q10) as a potential cytogenetic indicator of biallelic TP53 inactivation through double-hit mutations. These data suggest that MDS with der(5;19)(p10;q10) is clinically characterized by aberrant CD7 expression in blasts, a tendency for leukemic transformation, resistance to anti-leukemia therapies, and poor survival outcomes. We also noted that cases of der(5;19)(p10;q10) MDS/AML have been reported exclusively by Japanese institutions. Geographical and ethnic factors may contribute to oncogenesis, which can be triggered by exposure to alkylating agents.
不平衡的全臂易位der(5;19)(p10;q10)是骨髓增生异常肿瘤(MDS)和急性髓系白血病(AML)患者中一种罕见但反复出现的细胞遗传学异常。此前已报道了8例伴有der(5;19)(p10;q10)的MDS/AML病例。在此,我们描述了在我们机构的另外3例伴有der(5;19)(p10;q10)的MDS病例,我们通过下一代测序鉴定了髓系恶性肿瘤相关突变。所有患者均有两个TP53突变,每个突变的变异等位基因频率均>10%,提示双打击TP53突变。双打击TP53突变仅在约2%的MDS患者中发现,可能参与了细胞遗传学异常der(5;19)(p10;q10)、+19和复杂核型的发生,这些异常通常与接触烷化剂有关。我们提出der(5;19)(p10;q10)作为双打击突变导致双等位基因TP53失活的潜在细胞遗传学指标。这些数据表明,伴有der(5;19)(p10;q10)的MDS的临床特征为原始细胞中CD7表达异常、白血病转化倾向、对抗白血病治疗耐药以及生存预后不良。我们还注意到,der(5;19)(p10;q10) MDS/AML病例仅由日本机构报道。地理和种族因素可能促成肿瘤发生,这可能由接触烷化剂引发。