Additional acquisition of t(1;21)(p32;q22) in a patient relapsing with acute myelogenous leukemia with NUP98-HOXA9

被引：7

作者：

Aoki, Takatoshi ^{[2
]}

Miyamoto, Toshihiro ^{[1
]}

Yoshida, Shuro ^{[2
]}

Yamamoto, Asataro ^{[2
]}

Yamauchi, Takuji ^{[2
]}

Yoshimoto, Goichi ^{[2
]}

Mori, Yasuo ^{[2
]}

Kamezaki, Kenjiro ^{[2
]}

Iwasaki, Hiromi ^{[1
]}

Takenaka, Katsuto ^{[2
]}

Harada, Naoki ^{[2
]}

Nagafuji, Koji ^{[2
]}

Teshima, Takanori ^{[1
]}

Akashi, Koichi ^{[2
]}

机构：

[1] Kyushu Univ, Grad Sch Med Sci, Ctr Cellular & Mol Med, Higashi Ku, Fukuoka 8128582, Japan

[2] Kyushu Univ, Grad Sch Med Sci, Fukuoka 812, Japan

来源：

INTERNATIONAL JOURNAL OF HEMATOLOGY | 2008年 / 88卷 / 05期

关键词：

AML; t(1; 21); t(7; 11); NUP98-HOXA9; Clonal evolution;

D O I：

10.1007/s12185-008-0198-9

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

We report a 29-year-old Japanese male with acute myelogenous leukemia (AML)-M4 with a cryptic t(7;11)(p15;p15), in which a chimeric NUP98-HOXA9 fusion was detected by polymerase chain reaction analysis and a chromosomal analysis showed 46,XY. The patient received intensive chemotherapy and underwent autologous stem cell transplantation, and remission was confirmed by the disappearance of NUP98-HOXA9. However, 6 months after transplantation, the patient relapsed; NUP98-HOXA9 was detected again and karyotypic analysis revealed 46,XY, t(1;21)(p32;q22). Fluorescent in situ hybridization (FISH) analysis using an AML1-ETO translocation dual probe, showed that the 21q22 breakpoint involved AML1 locus. A retrospective FISH analysis showed that t(1;21) was absent at onset. This is the first reported case with AML who had a cryptic t(7;11)(p15;p15), and additionally acquired t(1;21) (p32;q22) at relapse.

引用

页码：571 / 574

页数：4

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