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Table 1 Correlation between residual γH2AX and cell killing in SiHa monolayers exposed to DNA damaging agents

From: Residual γH2AX foci as an indication of lethal DNA lesions

DNA damaging agent Mechanism of interaction with DNA Likely mechanism(s) of γH2AX formation aSlope (95% confidence limits) and correlation coefficient (r2)
X-rays SSB, DSB, base damage Direct DSBs 0.95 (0.57-1.33)
r 2 = 0.95
Etoposide Topo II inhibitor Direct DSBs 1.17 (0.91-1.44)
r 2 = 0.91
Temozolamide Base alkylation Base damage leading to DSBs during replicationb 0.62 (0.42-0.82)
r 2 = 0.82
MNNG Base alkylation Base damage leading to DSBs during replicationb 0.79 (0.52-1.07)
r 2 = 0.87
Cisplatin Inter- and intra-strand crosslinks Inter- and intra-strand crosslinks leading to DSBs during replicationb 0.77 (0.53-1.02)
r 2 = 0.87
Doxorubicin SSB, DSB, base damage, topo II inhibitor Direct DSBs and replication fork blockage leading to DSBs 0.95 (0.88-1.03)
r 2 = 0.99
Tirapazamine SSB, DSB, base damage, topo II inhibitor Direct DSBs and replication fork blockage leading to DSBs 1.06 (0.80-1.3)
r 2 = 0.90
Camptothecin Topo I inhibitor Replication fork blockage leading to DSBs 0.83 (0.61-1.04)
r 2 = 0.85
Hydrogen peroxide SSB Opposed single-strand breaks 1.06 (0.85-1.26)
r 2 = 0.93
  1. a The slope was obtained by plotting clonogenic surviving fraction versus the fraction of cells lacking foci.
  2. b After exposure to very high drug doses, γH2AX forms independently of cell cycle phase and may implicate opposed repair sites as responsible for triggering H2AX phosphorylation.