The oncogenic BCR/ABL tyrosine kinase induces constitutive enhanced 
"spontaneous" DNA damage and unfaithful repair in Philadelphia chromosome 
positive leukemia cells. Here, we investigated the changes of protein profile in 
H2O2-induced DNA damage/repair in BaF3-MIGR1 and BaF3-BCR/ABL cells through a 
proteomic strategy consisting of two-dimensional gel electrophoresis (2-DE) 
coupled with MALDI-TOF mass spectrometry. In total, 41 spots were differentially 
expressed and 13 proteins were identified with further MS analysis. Two 
essential proteins, Proto-oncogene tyrosine-protein kinase ABL1 (c-ABL) and Heat 
shock 70kDa protein 4 (Apg-2), were confirmed by Western blot and showed 
consistent changes with proteomic results. Moreover, functional analysis 
demonstrated that inhibition of Apg-2 not only decreased cell proliferation, but 
also induced cell apoptosis in BCR/ABL positive cells (BaF3-BCR/ABL, 
BaF3-BCR/ABL(T315I)). We also proved that Apg-2 inhibition aggravated H2O2 
induced damage in BCR/ABL positive cells, and enhanced the sensitivity of 
BaF3-BCR/ABL(T315I) to STI571. Taken together, the findings in this work provide 
us with some clues to a better understanding of the molecular mechanisms 
underlying BCR/ABL in the DNA damage/repair processes and demonstrated that 
Apg-2 would be a valid target for anti-leukemia drug development.