AML1 Amplification and 17q25 Deletion in a Case of Childhood Acute Lymphoblastic Leukemia

被引：8

作者：

Gulten, Tuna ^{[1
]}

Yakut, Tahsin ^{[1
]}

Karkucak, Mutlu ^{[1
]}

Baytan, Birol ^{[2
]}

Gunes, Adalet Meral ^{[2
]}

机构：

[1] Uludag Univ, Dept Med Genet, Fac Med, TR-16059 Gorukle, Bursa, Turkey

[2] Uludag Univ, Pediat Haematol Dept, Fac Med, TR-16059 Gorukle, Bursa, Turkey

来源：

JOURNAL OF CLINICAL LABORATORY ANALYSIS | 2009年 / 23卷 / 06期

关键词：

AML1; amplification; SEPT9; acute lymphoblastic leukemia; 17q25; aberration; ABNORMALITIES; GENES;

D O I：

10.1002/jcla.20343

中图分类号：

R446 [实验室诊断]; R-33 [实验医学、医学实验];

学科分类号：

1001 ;

摘要：

We report a case of childhood acute lymphoblastic leukemia (ALL) with both acute myeloid leukemia 1 (AML1) amplification and 17q25 deletion. AML1 gene is located on 21q22 and encodes a transcription factor. AML1 amplification is a common finding in childhood ALL, and itis observed as an increase in gene copy number by the FISH analysis. The mechanism of AML1 amplification is not associated with AML1 gene mutations. The 17q25 is a gene-rich chromosomal location and distinct abnormalities of this region have been observed in previous cases of different kinds of leukemia. Deletion of the 17q25 region has been reported in two leukemia patients. Septin 9 (SEPT9) and survivin genes are located on 17q25. High expression of these genes and AML1 amplification are regarded as markers in tumorigenesis and disease progression; however, more data are needed for accurate prognostic evaluation. J. Clin. Lab. Anal. 23:368-371, 2009. (C) 2009 Wiley-Liss, Inc.

引用

页码：368 / 371

页数：4

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