Identification of Gene Expression Signatures in Korean Acute Leukemia Patients.
- Author:
Kyung Hun LEE
1
;
Se Won PARK
;
Inho KIM
;
Sung Soo YOON
;
Seonyang PARK
;
Byoung Kook KIM
Author Information
1. Department of Internal Medicine, Seoul National University, College of Medicine, Korea. Seonpark@plaza.snu.ac.kr
- Publication Type:Original Article
- Keywords:
acute myeloid leukemia;
acute lymphoblastic leukemia;
microarray;
expression profiling
- MeSH:
Amyloid;
Antigens, CD79;
Antigens, CD9;
B-Lymphocytes;
Cathepsin C;
Diagnosis;
DNA Nucleotidylexotransferase;
Gene Expression*;
Genome;
Humans;
Leukemia*;
Leukemia, Myeloid, Acute;
Lymphoid Enhancer-Binding Factor 1;
Muramidase;
Peroxidase;
Precursor Cell Lymphoblastic Leukemia-Lymphoma;
Precursor Cells, B-Lymphoid;
Prostaglandin D2;
RNA;
Transcriptome*
- From:Genomics & Informatics
2006;4(3):97-102
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND: In acute leukemia patients, several successful methods of expression profiling have been used for various purposes, i.e., to identify new disease class, to select a therapeutic target, or to predict chemo-sensitivity and clinical outcome. In the present study, we tested the peripheral blood of 47 acute leukemia patients in an attempt to identify differentially expressed genes in AML and ALL using a Korean-made 10K oligo-nucleotide microarray. METHODS: Total RNA was prepared from peripheral blood and amplified for microarray experimentation. SAM (significant analysis of microarray) and PAM (prediction analysis of microarray) were used to select significant genes. The selected genes were tested for in a test group, independently of the training group. RESULTS: We identified 345 differentially expressed genes that differentiated AML and ALL patients (FWER < 0.05). Genes were selected using the training group (n=35) and tested for in the test group (n=12). Both training group and test group discriminated AML and ALL patients accurately. Genes that showed relatively high expression in AML patients were deoxynucleotidyl transferase, pre-B lymphocyte gene 3, B-cell linker, CD9 antigen, lymphoid enhancer-binding factor 1, CD79B antigen, and early B-cell factor. Genes highly expressed in ALL patients were annexin A 1, amyloid beta (A4) precursor protein, amyloid beta (A4) precursor-like protein 2, cathepsin C, lysozyme (renal amyloidosis), myeloperoxidase, and hematopoietic prostaglandin D2 synthase. CONCLUSION: This study provided genome wide molecular signatures of Korean acute leukemia patients, which clearly identify AML and ALL. Given with other reported signatures, these molecular signatures provide a means of achieving a molecular diagnosis in Korean acute leukemia patents.
