Abstract:
:Cancer cells show various types of mutations and aberrant expression in genes involved in DNA repair responses. These alterations induce genome instability and promote carcinogenesis steps and cancer progression processes. These defects in DNA repair have also been considered as suitable targets for cancer therapies. A most effective target so far clinically demonstrated is "homologous recombination repair defect", such as BRCA1/2 mutations, shown to cause synthetic lethality with inhibitors of poly(ADP-ribose) polymerase (PARP), which in turn is involved in DNA repair as well as multiple physiological processes. Different approaches targeting genomic instability, including immune therapy targeting mismatch-repair deficiency, have also recently been demonstrated to be promising strategies. In these DNA repair targeting-strategies, common issues could be how to optimize treatment and suppress/conquer the development of drug resistance. In this article, we review the extending framework of DNA repair response pathways and the potential impact of exploiting those defects on cancer treatments, including chemotherapy, radiation therapy and immune therapy.
journal_name
Semin Cancer Bioljournal_title
Seminars in cancer biologyauthors
Motegi A,Masutani M,Yoshioka KI,Bessho Tdoi
10.1016/j.semcancer.2019.02.005subject
Has Abstractpub_date
2019-10-01 00:00:00pages
29-46eissn
1044-579Xissn
1096-3650pii
S1044-579X(18)30089-0journal_volume
58pub_type
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journal_title:Seminars in cancer biology
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journal_title:Seminars in cancer biology
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journal_title:Seminars in cancer biology
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