As the hallmark of cancer, uncontrolled DNA replication confers excess proliferation capacity in cancer cells, it also consequently leads to replication stress, DNA breaks and genomic instability. Classic chemo-radiotherapy is aimed to kill cancer cells through induction of unrepairable DNA double-strand breaks (DSBs) that arrest DNA replication and division machinery and it is widely used in clinical practices. As a consequence, molecular mechanisms and cellular pathways that are implicated in the regulation of DNA repair, DNA replication restart, DNA damage response, DNA metabolism, et al. are highly associated with cancer cell sensitivity to cancer chemo-radiotherapies. Meanwhile, modulating DNA repair capacity could otherwise affect cancer treatments.
In view of the importance of DNA repair, DNA metabolism and replication in cancer therapies, intense efforts have been made to develop cancer drugs targeting these biological processes. Many anti-cancer drugs currently used in clinical practice are designed to target the critical components involved in these DNA related functions. For instance, platinum-based cancer drugs cause interstrand DNA-DNA cross-links, which subsequently block DNA replication and induce DNA breaks. It is worth noting that DNA repair protein poly (ADP-ribose) polymerase (PARP) inhibitor, which is the first-line maintenance treatment for BRCA1/2 mutant ovarian, breast, prostate and pancreatic cancer, is the first approved anti-cancer agent utilizing synthetic lethality. PARP inhibitors selectively kill homologous recombination (HR) repair deficiency cancer cells, therefore, HR repair capacity in cancer cells is considered not only an important biomarker to predict PARP inhibitor sensitivity, but also a critical drug target to optimize PARP inhibitor treatment. The success of PARP inhibitors and traditional chemotherapies have made DNA repair, DNA metabolism and replication hot drug targets for cancer therapeutics.
This topic aims to publish articles including up-to-date scientific research articles, inspiring opinions, and comprehensive reviews on the field of DNA repair, replication, DNA metabolism, and Radio-chemoresistance. And we aim to promote our understanding and knowledge in this field by encouraging active communication within the research communities of biological and medical science, with an emphasis on the application in clinical cancer therapies. We welcome Original Research and Review articles covering, but not limited to, the following:
(1) New DNA repair mechanisms that can be targeted in the treatment of cancer.
(2) Novel therapeutic strategies to enhance outcomes and avoid side effects for traditional chemotherapies.
(3) New strategies for cancer therapy utilizing replication stress and DNA damage.
(4) Novel DNA damage and repair biomarkers for prediction of cancer sensitivity for targeted therapies and immunotherapies.
(5) Studies of DNA repair, metabolism, and replication related gene signatures that can predict cancer prognosis and progression.
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.
As the hallmark of cancer, uncontrolled DNA replication confers excess proliferation capacity in cancer cells, it also consequently leads to replication stress, DNA breaks and genomic instability. Classic chemo-radiotherapy is aimed to kill cancer cells through induction of unrepairable DNA double-strand breaks (DSBs) that arrest DNA replication and division machinery and it is widely used in clinical practices. As a consequence, molecular mechanisms and cellular pathways that are implicated in the regulation of DNA repair, DNA replication restart, DNA damage response, DNA metabolism, et al. are highly associated with cancer cell sensitivity to cancer chemo-radiotherapies. Meanwhile, modulating DNA repair capacity could otherwise affect cancer treatments.
In view of the importance of DNA repair, DNA metabolism and replication in cancer therapies, intense efforts have been made to develop cancer drugs targeting these biological processes. Many anti-cancer drugs currently used in clinical practice are designed to target the critical components involved in these DNA related functions. For instance, platinum-based cancer drugs cause interstrand DNA-DNA cross-links, which subsequently block DNA replication and induce DNA breaks. It is worth noting that DNA repair protein poly (ADP-ribose) polymerase (PARP) inhibitor, which is the first-line maintenance treatment for BRCA1/2 mutant ovarian, breast, prostate and pancreatic cancer, is the first approved anti-cancer agent utilizing synthetic lethality. PARP inhibitors selectively kill homologous recombination (HR) repair deficiency cancer cells, therefore, HR repair capacity in cancer cells is considered not only an important biomarker to predict PARP inhibitor sensitivity, but also a critical drug target to optimize PARP inhibitor treatment. The success of PARP inhibitors and traditional chemotherapies have made DNA repair, DNA metabolism and replication hot drug targets for cancer therapeutics.
This topic aims to publish articles including up-to-date scientific research articles, inspiring opinions, and comprehensive reviews on the field of DNA repair, replication, DNA metabolism, and Radio-chemoresistance. And we aim to promote our understanding and knowledge in this field by encouraging active communication within the research communities of biological and medical science, with an emphasis on the application in clinical cancer therapies. We welcome Original Research and Review articles covering, but not limited to, the following:
(1) New DNA repair mechanisms that can be targeted in the treatment of cancer.
(2) Novel therapeutic strategies to enhance outcomes and avoid side effects for traditional chemotherapies.
(3) New strategies for cancer therapy utilizing replication stress and DNA damage.
(4) Novel DNA damage and repair biomarkers for prediction of cancer sensitivity for targeted therapies and immunotherapies.
(5) Studies of DNA repair, metabolism, and replication related gene signatures that can predict cancer prognosis and progression.
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.
