The comparative analysis of serum proteomes for the discovery of biomarkers for acute myeloid leukemia

Acute myeloid leukemia (AML) develops as the consequence of a series of genetic changes in a hematopoietic precursor cell. However, the definitive diagnostic protein biomarkers for AML are still unclear. In our study to identify the biomarkers for an initial diagnosis, detection of relapse, and moni...

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Published inExperimental hematology Vol. 32; no. 9; pp. 836 - 842
Main Authors Kwak, Jae-Yong, Ma, Tian-Ze, Yoo, Min-Jeong, Hee Choi, Bok, Kim, Han-Gyu, Kim, So-Ri, Yim, Chang-Yeol, Kwak, Yong-Geun
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier Inc 01.09.2004
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Summary:Acute myeloid leukemia (AML) develops as the consequence of a series of genetic changes in a hematopoietic precursor cell. However, the definitive diagnostic protein biomarkers for AML are still unclear. In our study to identify the biomarkers for an initial diagnosis, detection of relapse, and monitoring the minimal residual disease in AML by a less invasive method, serum proteins reflecting alterations in their proteomes were analyzed. We compared the two-dimensional electrophoresis patterns of human sera of 12 patients with AML with those of 12 normal subjects. The differentially expressed spots were identified by matrix-assisted laser desorption/ionization time-of-flight and electrospray ionization quadupole time-of-flight mass spectrometries. Eight proteins that expressed differentially in the AML group were found. The expression levels of α-2-HS-glycoprotein, complement-associated protein SP-40, 40, RBP4 gene product, lipoprotein C-III, and an unknown protein were downregulated in serum of AML patients, whereas the other three proteins, including immunoglobulin heavy-chain variant, proteosome 26S ATPase subunit 1, and haptoglobin-1 were upregulated. These results suggest that these proteins can be used as less invasive diagnostic and monitoring biomarkers of AML if further studies are done.
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ISSN:0301-472X
1873-2399
DOI:10.1016/j.exphem.2004.06.006