The incidence of TP53 mutation among MLL-rearranged ALL cell lines and t(1;19)-ALL cell lines was 60% (6/10) and 66.7% (4/6), respectively, while that among Ph1-positive ALL cell lines and t(17;19)-ALL cell lines was 14.3% (1/7) and 0% (0/4), respectively (Fig. 1B) . Of note, consistent with the series of clinical samples in previous reports [5] [6] [7] , the incidence of TP53 mutation among MLL-rearranged and t(1;19)-positive ALL cell lines was significantly higher than that among the other ALL cell lines including Ph1 and t(17;19)-positive ALL cell lines (P < 0.05, chi-squared test). Although the number of cell lines analyzed is limited, this is the first direct observation in a single analysis of the correlation between the incidence of TP53 mutation and types of translocation in B-precursor ALLs. The incidence of TP53 mutation among MLL-rearranged and t(1;19)-positive ALL cell lines observed in this study was higher than that in previous reports using clinical samples, suggesting that TP53 mutation plays a role in disease progression and/or the in vitro proliferative activity of MLL-rearranged and t(1;19)-positive ALL but not necessarily Ph1 and t(17;19)-positive ALL. It should be noted that E2A-HLF chimera derived from t (17;19) has the potential to protect cells from apoptosis induced by activation of the p53 pathway [20] , suggesting that E2A-HLF might overcome at least the proapoptotic activity of p53. Similarly, it was reported that BCR-ABL blocks apoptotic cell death induced by DNA damage without altering p53-dependent G1 arrest [21] . Thus, E2A-HLF and BCR-ABL may have the potential to overcome the pro-apoptotic activity of p53 and, thus, TP53 mutation is not necessary for disease progression. In other words, regardless of the TP53 gene status, Ph1-positive ALL and t(17;19)-ALL could be relatively resistant to therapeutic modalities that activate the p53 pathway such as irradiation. In contrast, without TP53 mutation, MLL-rearranged ALL and t(1;19)-ALL might be relatively sensitive to therapeutic modalities that activate the p53 pathway, and, thus, TP53 mutation could be one of the prognostic factors for therapeutic outcome in these leukemias.