Sea-Blue Histiocytosis of Bone Marrow in a Patient with t(8;22) Acute Myeloid Leukemia
Sea-Blue Histiocytosis of Bone Marrow in a Patient with t(8;22) Acute Myeloid Leukemia
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t(8;22) 急性髓系白血病患者骨髓海蓝色组织细胞增多症
DOI：
10.1159/000508495
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发表时间：
2020
影响因子：
0.8
通讯作者：
Uemura Makiko
中科院分区：
文献类型：
--
作者：
Imataki Osamu;Uemura Makiko
一名80岁的日本男性接受了由环磷酰胺、多柔比星、长春新碱和泼尼松龙组成的化疗，治疗非霍奇金淋巴瘤。化疗后9个月，他被诊断为急性髓性白血病（AML）（M4），伴有8 p11和22 q13易位。患者骨髓显示明显程度的海蓝色组织细胞增生症。他的病很严重，他死于这种疾病。海蓝色组织细胞是具有蓝色空泡和颗粒沉积的巨噬细胞，其由死亡细胞的吞噬作用和随后的磷脂沉积引起。AML伴t（8; 22）（p11; q13）易位是AML的一种罕见亚型，在所有AML病例中的患病率低于1.0%。t（8; 22）（p11; q13）的肿瘤发生由单核细胞白血病锌指蛋白（MOZ）和转录因子p300的融合蛋白引起。MOZ可以与各种易位靶点融合，包括CBT、TIF 2和p300，分别对应于t（8; 16）、inv（8）和t（8; 22）。该AML亚组揭示了该疾病的特征，包括单核细胞停滞和原始细胞的巨噬细胞/噬血细胞作用。携带MOZ作为异常融合基因的AML M4/M5亚型的相当大比例表现为红细胞吞噬作用。虽然罕见，t（8; 22）对AML M4/M5亚型非常特异，并且似乎代表海蓝色组织细胞增生症作为具有巨噬细胞活化的单核细胞AML的特征性特征之一。因此，海蓝色组织细胞被认为是MOZ易位的单核细胞AML的标志之一。
An 80-year-old Japanese male was treated with chemotherapy consisting of cyclophosphamide, doxorubicin, vincristine, and prednisolone, for non-Hodgkin lymphoma. Nine months after the chemotherapy, he was diagnosed with acute myeloid leukemia (AML)(M4) with translocation 8p11 and 22q13. The patient bone marrow indicated a remarkable degree of sea-blue histiocytosis. His disease was aggressive, and he died of the disease. Sea-blue histiocytes are macrophages harboring blue vacuoles and granular deposition, which results from the phagocytosis of dead cells and the subsequent deposition of phospholipids. AML with the t (8; 22)(p11; q13) translocation is a rare subtype of AML, which is a rare translocation with a prevalence of less than 1.0% among all AML cases. The oncogenesis of t (8; 22)(p11; q13) is caused by the fusion protein monocytic leukemia zinc finger protein (MOZ) and transcription factor p300. MOZ can be fused to various translocation targets including CBT, TIF2, and p300, corresponding to t (8; 16), inv (8), and t (8; 22), respectively. This subgroup of AML reveals the hallmarks of the disease, including monocytic arrest and erythro/hemophagocytosis by blasts. A substantial proportion of the AML M4/M5 subtype harboring MOZ as an aberrant fusion gene represents erythrophagocytosis. Although rare, t (8; 22) is very specific to the AML M4/M5 subtype and seems to represent sea-blue histiocytosis as one of the characteristic features of monocytic AML with macrophage activation. Thus, sea-blue histiocytes are considered to be one of hallmarks in monocytic AML with MOZ translocation.