DNA repair dysregulation from cancer driver to therapeutic target

By N. Curtin. Nature Reviews. Cancer, 2012

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Laying a trap to kill cancer cells: PARP inhibitors and their mechanisms of action (2016, background): “Although O6 methylation is the main mechanism of action for temozolomide in glioblastomas, which commonly lack MGMT (O6-guanine-methyl-transferase), N7 guanine methylation is the most prevalent lesion and is efficiently dealt with by PARP1mediated repair (62).”
Drug Resistance in Cancer: An Overview (2014, background): “O6-benzylguanine sensitize healthy cells to cytotoxic drugs [54,59,60].”
Revisiting the hallmarks of cancer. (2017, positive): “Some of the most notable familial cancer syndromes entail germline mutations involving DNA repair lators in the cancer context, the disruption of which (over-reliance on an upregulated pathway or defects in another) serves overall tumor survival and progression, but may also represent a vulnerabilit”
ROS and the DNA damage response in cancer (2018, background): “DNA can be damaged by a variety of exogenous and endogenous insults including chemicals, radiation, free radicals, and topological changes, each causing distinct forms of damage [1].”
Homologous recombination deficiency: Exploiting the fundamental vulnerability of ovarian cancer (2015, background): “Two of the PI3K-related protein kinases, Ataxia-telangiectasia mutated (ATM) and Ataxiatelangiectasia and RAD3-related (ATR), occupy a central role in signaling DNA damage to cell-cycle checkpoints and DNA repair pathways (128).”