Study on the Mechanisms of CML Blast Crisis by Comparative Proteome Analysis.

The clinical course of chronic myeloid leukemia(CML)is characteristically triphasic, comprising chronic and accelerated phases and blast crisis. Chronic phase(CP) is characterized by the Ph chromosome as the sole genetic abnormality and blast crisis(BC), which is the terminal phase of CML, often associated with additional chromosomal and molecular secondary changes. Although CML is probably the most extensively studied human malignancy, the mechanisms of CML blast crisis are still poorly understood. In current study, we analyzed the changes of protein expression between CML-CP(25 cases) and CML-BC(20 cases) by Two-dimensional polyacrylamide gel electrophoresis(2-D PAGE). Compared with that of CML-CP, 33 proteins’ intensities of CML-BC were found to have significant difference including 23 increasing and 13 decreasing. 15 proteins were identified by peptide mass fingerprint in combination with database searching including proteasome activator complex, hnRNP, annexin A4, serine proteinase inhibitor, annexin A1, GAPDH, RhoGDI, enolase, proteasome subunit 6a, GTP binding protein, leukotriene A4 hydrolase, Rac-RhoGDI, thioredoxin, proteasome subunit 4β and DJ-1 protein, and the functions of these proteins involve cell signal transduction, apoptosis, proliferation and transcription. In conclusion, our study provided a profile of protein expression difference between CML-CP and CML-BC and contributed to understand the mechanisms of CML blast crisis.