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- W2783267568 abstract "The human genome is under constant stress from thousands of DNA damage lesions that are formed as indirect products of endogenous metabolic or enzymatic processes, or generated from exposure to exogenous environmental physical and chemical agents. A number of highly conserved DNA repair pathways have evolved to identify and resolve these lesions, preventing a collection of potentially deleterious consequences. At the molecular level, DNA damage can arrest RNA transcription or DNA replication processes, or can lead to mutagenic by-pass or gross chromosomal rearrangement events. At the cellular level, such outcomes can result in apoptosis, senescence, or transformation, consequences known to underlie disease and aging. Consistently, germline and somatic mutations at DNA repair gene loci, as well as epigenetic inactivation or loss of heterozygosity, have been linked to an array of cancer diagnoses, including familial cancer syndromes, polymorphism-associated predispositions, and sporadic malignancies, as well as to neurological disease and premature aging features. DNA damage also plays an important role in the cytotoxicity of numerous cancer treatments, namely those involving radiotherapy or commonly used chemotherapeutic drugs. More recently, molecular targets within DNA repair pathways have been the focus of drug development efforts, both as possible potentiators of existing anticancer agents, and as targeted monotherapies within a synthetic lethality paradigm." @default.
- W2783267568 created "2018-01-26" @default.
- W2783267568 creator A5067311031 @default.
- W2783267568 creator A5068693127 @default.
- W2783267568 creator A5073739028 @default.
- W2783267568 date "2018-01-01" @default.
- W2783267568 modified "2023-09-26" @default.
- W2783267568 title "Role of DNA Repair in Carcinogenesis and Cancer Therapeutics" @default.
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