Yamamoto Katsuya, Kawamoto Shinichiro, Mizutani Yu, Yakushijin Kimikazu, Yamashita Tomoe, Nakamachi Yuji, Kawano Seiji, Hayashi Yoshitake, Matsuoka Hiroshi, Minami Hironobu
Division of Medical Oncology/Hematology, Department of Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
Cytogenet Genome Res. 2016;149(3):165-170. doi: 10.1159/000448447. Epub 2016 Sep 9.
The t(12;17)(p13;q11∼21) translocation is a very rare but recurrent cytogenetic aberration observed predominantly in early pre-B acute lymphoblastic leukemia (ALL) with CD19+CD10-CD33+ phenotype. This translocation was shown to form a fusion gene between TAF15 at 17q12 and ZNF384 at 12p13. On the other hand, der(1;18)(q10;q10) has been detected as a rare unbalanced whole-arm translocation leading to trisomy 1q in myeloid malignancies. We describe here the first case of mixed phenotype acute leukemia (MPAL) with a t(12;17)(p13;q21)/TAF15-ZNF384, which also had der(1;18)(q10;q10) as an additional abnormality. A 74-year-old woman was diagnosed with MPAL, B/myeloid, because bone marrow blasts were positive for myeloperoxidase, CD19, and CD22. Chromosome analysis showed 46,XX, +1,der(1;18)(q10;q10),t(2;16)(q13;q13),t(12;17)(p13;q21). Expression of the TAF15-ZNF384 fusion transcript was confirmed: TAF15 exon 6 was fused in-frame to ZNF384 exon 3. This type of fusion gene has been reported in 1 acute myeloid leukemia case and 3 ALL cases. Thus, at present, it is difficult to find a specific association between the structure of the TAF15-ZNF384 fusion gene and the leukemia phenotype. The TAF15-ZNF384 fusion may occur in early common progenitor cells that could differentiate into both the myeloid and lymphoid lineages. Furthermore, der(1;18)(q10;q10) might play some role in the appearance of an additional myeloid phenotype.
t(12;17)(p13;q11∼21)易位是一种非常罕见但反复出现的细胞遗传学异常,主要见于具有CD19+CD10-CD33+表型的早期前B急性淋巴细胞白血病(ALL)。这种易位被证明会在17q12的TAF15和12p13的ZNF384之间形成一个融合基因。另一方面,der(1;18)(q10;q10)已被检测为一种罕见的不平衡全臂易位,导致髓系恶性肿瘤中出现1q三体。我们在此描述了首例伴有t(12;17)(p13;q21)/TAF15-ZNF384的混合表型急性白血病(MPAL)病例,该病例还存在额外异常der(1;18)(q10;q10)。一名74岁女性被诊断为MPAL,B/髓系,因为骨髓原始细胞髓过氧化物酶、CD19和CD22呈阳性。染色体分析显示为46,XX, +1,der(1;18)(q10;q10),t(2;16)(q13;q13),t(12;17)(p13;q21)。TAF15-ZNF384融合转录本的表达得到确认:TAF15外显子6与ZNF384外显子3框内融合。这种类型的融合基因已在1例急性髓系白血病病例和3例ALL病例中报道过。因此,目前很难找到TAF15-ZNF384融合基因的结构与白血病表型之间的特定关联。TAF15-ZNF384融合可能发生在早期共同祖细胞中,这些祖细胞可分化为髓系和淋巴系。此外,der(1;18)(q10;q10)可能在额外髓系表型的出现中起一定作用。