DNA Damage Repair: Predictor of Platinum Efficacy in Ovarian Cancer?

Ovarian cancer (OC) is the seventh most common type of cancer in women worldwide. Treatment for OC usually involves a combination of surgery and chemotherapy with carboplatin and paclitaxel. Platinum-based agents exert their cytotoxic action through development of DNA damage, including the formation...

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Main Authors: Dimitra T. Stefanou, Vassilis L. Souliotis, Roubini Zakopoulou, Michalis Liontos, Aristotelis Bamias
Format: Article
Language:English
Published: MDPI AG 2021-12-01
Series:Biomedicines
Subjects:
Online Access:https://www.mdpi.com/2227-9059/10/1/82
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author Dimitra T. Stefanou
Vassilis L. Souliotis
Roubini Zakopoulou
Michalis Liontos
Aristotelis Bamias
author_facet Dimitra T. Stefanou
Vassilis L. Souliotis
Roubini Zakopoulou
Michalis Liontos
Aristotelis Bamias
author_sort Dimitra T. Stefanou
collection DOAJ
description Ovarian cancer (OC) is the seventh most common type of cancer in women worldwide. Treatment for OC usually involves a combination of surgery and chemotherapy with carboplatin and paclitaxel. Platinum-based agents exert their cytotoxic action through development of DNA damage, including the formation of intra- and inter-strand cross-links, as well as single-nucleotide damage of guanine. Although these agents are highly efficient, intrinsic and acquired resistance during treatment are relatively common and remain a major challenge for platinum-based therapy. There is strong evidence to show that the functionality of various DNA repair pathways significantly impacts tumor response to treatment. Various DNA repair molecular components were found deregulated in ovarian cancer, including molecules involved in homologous recombination repair (HRR), nucleotide excision repair (NER), mismatch repair (MMR), non-homologous end-joining (NHEJ), and base excision repair (BER), which can be possibly exploited as novel therapeutic targets and sensitive/effective biomarkers. This review attempts to summarize published data on this subject and thus help in the design of new mechanistic studies to better understand the involvement of the DNA repair in the platinum drugs resistance, as well as to suggest new therapeutic perspectives and potential targets.
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spelling doaj.art-775daf14f30c4e1cb70cd7d4a96d00482023-11-23T13:03:29ZengMDPI AGBiomedicines2227-90592021-12-011018210.3390/biomedicines10010082DNA Damage Repair: Predictor of Platinum Efficacy in Ovarian Cancer?Dimitra T. Stefanou0Vassilis L. Souliotis1Roubini Zakopoulou2Michalis Liontos3Aristotelis Bamias4First Department of Medicine, Laiko General Hospital, School of Medicine, National and Kapodistrian University of Athens, 11527 Athens, GreeceInstitute of Chemical Biology, National Hellenic Research Foundation, 11635 Athens, Greece2nd Propaedeutic Department of Internal Medicine, Attikon University Hospital, National and Kapodistrian University of Athens, 12462 Athens, GreeceDepartment of Clinical Therapeutics, Alexandra General Hospital, School of Medicine, National and Kapodistrian University of Athens, 11528 Athens, Greece2nd Propaedeutic Department of Internal Medicine, Attikon University Hospital, National and Kapodistrian University of Athens, 12462 Athens, GreeceOvarian cancer (OC) is the seventh most common type of cancer in women worldwide. Treatment for OC usually involves a combination of surgery and chemotherapy with carboplatin and paclitaxel. Platinum-based agents exert their cytotoxic action through development of DNA damage, including the formation of intra- and inter-strand cross-links, as well as single-nucleotide damage of guanine. Although these agents are highly efficient, intrinsic and acquired resistance during treatment are relatively common and remain a major challenge for platinum-based therapy. There is strong evidence to show that the functionality of various DNA repair pathways significantly impacts tumor response to treatment. Various DNA repair molecular components were found deregulated in ovarian cancer, including molecules involved in homologous recombination repair (HRR), nucleotide excision repair (NER), mismatch repair (MMR), non-homologous end-joining (NHEJ), and base excision repair (BER), which can be possibly exploited as novel therapeutic targets and sensitive/effective biomarkers. This review attempts to summarize published data on this subject and thus help in the design of new mechanistic studies to better understand the involvement of the DNA repair in the platinum drugs resistance, as well as to suggest new therapeutic perspectives and potential targets.https://www.mdpi.com/2227-9059/10/1/82ovarian cancerDNA repairplatinum drugseffective biomarkerstherapeutic targets
spellingShingle Dimitra T. Stefanou
Vassilis L. Souliotis
Roubini Zakopoulou
Michalis Liontos
Aristotelis Bamias
DNA Damage Repair: Predictor of Platinum Efficacy in Ovarian Cancer?
Biomedicines
ovarian cancer
DNA repair
platinum drugs
effective biomarkers
therapeutic targets
title DNA Damage Repair: Predictor of Platinum Efficacy in Ovarian Cancer?
title_full DNA Damage Repair: Predictor of Platinum Efficacy in Ovarian Cancer?
title_fullStr DNA Damage Repair: Predictor of Platinum Efficacy in Ovarian Cancer?
title_full_unstemmed DNA Damage Repair: Predictor of Platinum Efficacy in Ovarian Cancer?
title_short DNA Damage Repair: Predictor of Platinum Efficacy in Ovarian Cancer?
title_sort dna damage repair predictor of platinum efficacy in ovarian cancer
topic ovarian cancer
DNA repair
platinum drugs
effective biomarkers
therapeutic targets
url https://www.mdpi.com/2227-9059/10/1/82
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AT vassilislsouliotis dnadamagerepairpredictorofplatinumefficacyinovariancancer
AT roubinizakopoulou dnadamagerepairpredictorofplatinumefficacyinovariancancer
AT michalisliontos dnadamagerepairpredictorofplatinumefficacyinovariancancer
AT aristotelisbamias dnadamagerepairpredictorofplatinumefficacyinovariancancer