Higuchi Masakazu, Sasaki Shoichi, Kawadoko Shin-Ichiro, Uchiyama Hikaru, Yasui Takaharu, Kamihira Takashi, Aoki Ken-Ichi, Sasaguri Takakazu, Nakano Ryuji, Uchiyama Akihiko, Muta Tsuyoshi, Ohshima Koichi
Department of Internal Medicine, Japan Community Health Care Organization (JCHO) Kyushu Hospital, Fukuoka, Japan.
Department of Hematology, JR Kyushu Hospital, 1-1, Takada 2-chome, Moji-ku, Kitakyushu, Fukuoka, 800-0031, Japan.
Int J Hematol. 2015 Oct;102(4):482-7. doi: 10.1007/s12185-015-1802-4. Epub 2015 May 8.
Secondary non-Hodgkin lymphoma following acute myeloid leukemia (AML) is extremely rare. We here describe a unique case involving a patient who developed Epstein-Barr virus (EBV)-positive diffuse large B-cell lymphoma (DLBCL) during complete remission (CR) of AML. A 75-year-old Japanese man was initially diagnosed with AML with maturation (FAB M2), bearing chromosomal translocation t(3,4)(p25;q21). After intensive chemotherapy, bone marrow aspiration revealed normal karyotype, and he achieved CR. Six years and 4 months later, he was still in CR from AML, but developed DLBCL presenting in the terminal ileum. Cytogenetic analysis of the DLBCL cells showed the same translocation as the previous AML. The rearrangements of the immunoglobulin heavy chain genes of the two malignancies were examined using polymerase chain reaction amplification, and the rearrangement patterns were found to differ from each other. Our data thus suggest that, in the present case, the AML and DLBCL arose from a common progenitor cell, as indicated by the clonal abnormality t(3,4)(p25;q21), and that different immunoglobulin heavy chain gene rearrangements occurred during each course of clonal evolution.
急性髓系白血病(AML)后发生的继发性非霍奇金淋巴瘤极为罕见。我们在此描述一例独特病例,患者在AML完全缓解(CR)期间发生了爱泼斯坦-巴尔病毒(EBV)阳性弥漫性大B细胞淋巴瘤(DLBCL)。一名75岁日本男性最初被诊断为伴有成熟的AML(FAB M2),存在染色体易位t(3,4)(p25;q21)。强化化疗后,骨髓穿刺显示核型正常,他达到了CR。6年零4个月后,他仍处于AML的CR状态,但发生了以回肠末端为表现部位的DLBCL。对DLBCL细胞进行细胞遗传学分析显示与先前的AML有相同的易位。使用聚合酶链反应扩增检测了两种恶性肿瘤免疫球蛋白重链基因的重排,发现重排模式彼此不同。因此我们的数据表明,在本病例中,如克隆异常t(3,4)(p25;q21)所示,AML和DLBCL起源于共同的祖细胞,并且在克隆进化的每个过程中发生了不同的免疫球蛋白重链基因重排。