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Fig. 1 | Journal of Biomedical Science

Fig. 1

From: Dissecting the mechanism of temozolomide resistance and its association with the regulatory roles of intracellular reactive oxygen species in glioblastoma

Fig. 1

Schema of classical model of the pharmacology mechanism causing temozolomide (TMZ) resistance. Methylation of O6, N3, and N7 in DNA can be modulated by the drug. Repairing response through DDR can cause divergent results. As the notable factor targeting majorly on O6-methylguanine, presence of MGMT leads to salvage for the cells to survive, and thus, will have negative impact to drug susceptibility in terms of the drug effect. Without adequate rescuing action, futile repairment will lead to single- or double-strand break, leading to associated reaction causing cell death. Me methylation, SSB single-strand break, DSB double-strand break, BER base excision repair, MPG N-methylpurine DNA glycosylase

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