Suppr超能文献

伴有t(12;17)(p13;q21)/TAF15-ZNF384及其他染色体异常的混合表型急性白血病

Mixed Phenotype Acute Leukemia with t(12;17)(p13;q21)/TAF15-ZNF384 and Other Chromosome Abnormalities.

作者信息

Yamamoto Katsuya, Kawamoto Shinichiro, Mizutani Yu, Yakushijin Kimikazu, Yamashita Tomoe, Nakamachi Yuji, Kawano Seiji, Hayashi Yoshitake, Matsuoka Hiroshi, Minami Hironobu

机构信息

Division of Medical Oncology/Hematology, Department of Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.

出版信息

Cytogenet Genome Res. 2016;149(3):165-170. doi: 10.1159/000448447. Epub 2016 Sep 9.

Abstract

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.

摘要

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。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验