Mass spectrography analysis of differential proteome in childhood TEL/AML1-positive acute lymphoblastic leukemia.
- Author:
Ye GUO
1
;
Bao-Li FAN
;
Yu-Mei CHEN
;
Ying HU
;
Yao ZOU
;
Xiao-Juan CHEN
;
Li ZHANG
;
Xiao-Fan ZHU
Author Information
1. Diagnostic and Therapeutic Center for Childhoood Hematologic Diseases, Institute of Hematology & Hospital of Blood Diseases, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjing 300020, China.
- Publication Type:Journal Article
- MeSH:
Child;
Child, Preschool;
Core Binding Factor Alpha 2 Subunit;
genetics;
metabolism;
Female;
Humans;
Male;
Mass Spectrometry;
Oncogene Proteins, Fusion;
genetics;
metabolism;
Precursor Cell Lymphoblastic Leukemia-Lymphoma;
genetics;
metabolism;
Proteome
- From:
Journal of Experimental Hematology
2010;18(1):116-121
- CountryChina
- Language:Chinese
-
Abstract:
The study was aimed to establish differential proteomic expression analysis of two dimensional electrophoresis and mass spectrography, and to further explore the mechanisms of nosogenesis in childhood TEL/AML1(+) acute lymphoblastic leukemia. On the basis of initial leukocyte count and prognostic factors, patients enrolled in this study were divided into three risk groups (early relapse, high leukocyte count and standard risk groups). The proteins of leukemic cells from patients at diagnosis were separated by two-dimensional gel electrophoresis. Spot detection, quantification and alignment were performed with the PDQuest 7.3.0 image analysis software. Differentially expressed spots were analyzed by mass spectrometry for peptide mass finger (PMF) data. The results showed that the significant difference of protein expression profile existed in 3 groups of childhood TEL/AML1-positive acute lymphoblastic leukemia. Compared with the high leukocyte count and standard risk groups, 71 protein spots disappeared; 93 new protein spots were found; 37 protein spot expressions were up-regulated; 23 protein spots were down-regulated in early relapse group. Compared the high leukocyte count group, 6 protein spots disappeared, 56 new protein spots were found, 7 protein spot expression were up-regulated, 19 protein spot expressions were down-regulated in standard risk group. The identification of 40 differential protein spots by using mass spectrometry revealed some proteins in 3 groups such as tropomyosin, lactotransferrin, lactate dehydrogenase A, CRMP1 protein, alphaenolase, AKR1B1, calnexin precursor, heat shock protein (HSP86/HSP89/HSP90), annexin VI, G22P1 and so on. Among them the HSP86/HSP89/HSP90 highly expressed only in early reapse group, the lactotransferrin, alphenolase and G22P1 expressions were up-regulated in early relapse group. It is concluded that the protein expression in early relapse group is significant different from the others. Some proteins may be further used in research on leukemia mechanisms. In addition, these analyses may promote the identification of new targets for individualized treatment approaches.
