Figure 5.
Figure 5. The effects of ATM and TP53 mutations on damage-induced apoptosis measured by cleavage of PARP1. (A) The percentage of the initial PARP1 remaining at 24 hours after IR was plotted for each tumor in each genetic category. There was no activation of apoptosis, as indicated by the 100% remaining uncleaved PARP1. Median values for the percentage of PARP1 remaining at 24 hours are shown for all genetic subgroups and were statistically significantly different (P = .019). (B) In CLLs 122 and 53, with wild-type ATM and TP53 genes, there was cleavage of PARP1 at both 8 and 24 hours after irradiation, reaching a maximum at 24 hours. In CLL 124, with one ATM mutation and one TP53 mutation, PARP1 cleavage was absent even at 24 hours.

The effects of ATM and TP53 mutations on damage-induced apoptosis measured by cleavage of PARP1. (A) The percentage of the initial PARP1 remaining at 24 hours after IR was plotted for each tumor in each genetic category. There was no activation of apoptosis, as indicated by the 100% remaining uncleaved PARP1. Median values for the percentage of PARP1 remaining at 24 hours are shown for all genetic subgroups and were statistically significantly different (P = .019). (B) In CLLs 122 and 53, with wild-type ATM and TP53 genes, there was cleavage of PARP1 at both 8 and 24 hours after irradiation, reaching a maximum at 24 hours. In CLL 124, with one ATM mutation and one TP53 mutation, PARP1 cleavage was absent even at 24 hours.

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