DNA Damage Response

Oksenych, Valentyn; Kainov, Denis E.

doi:10.3390/biom11010123

Cited by 3 publications

(2 citation statements)

References 23 publications

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“…The third class encompasses nucleotide excision repair (NER), which has evolved to combat DNA damage leading to distortion of the DNA helical structure, such as UV-induced lesions or chemical cross-linking ( 35 ). NER is the most important pathway among these repair pathways and can repair cellular damage caused by DNA double helix distortion ( 36 – 39 ).…”

Section: The Ercc4 Gene and Its Biological Functionsmentioning

confidence: 99%

ERCC4: a potential regulatory factor in inflammatory bowel disease and inflammation-associated colorectal cancer

Shi,

Wang,

Jiang

et al. 2024

Front. Endocrinol.

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The pathogenesis of inflammatory bowel disease (IBD) remains unclear and is associated with an increased risk of developing colitis-associated cancer (CAC). Under sustained inflammatory stimulation in the intestines, loss of early DNA damage response genes can lead to tumor formation. Many proteins are involved in the pathways of DNA damage response and play critical roles in protecting genes from various potential damages that DNA may undergo. ERCC4 is a structure-specific endonuclease that participates in the nucleotide excision repair (NER) pathway. The catalytic site of ERCC4 determines the activity of NER and is an indispensable gene in the NER pathway. ERCC4 may be involved in the imbalanced process of DNA damage and repair in IBD-related inflammation and CAC. This article primarily reviews the function of ERCC4 in the DNA repair pathway and discusses its potential role in the processes of IBD-related inflammation and carcinogenesis. Finally, we explore how this knowledge may open novel avenues for the treatment of IBD and IBD-related cancer.

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Section: The Ercc4 Gene and Its Biological Functionsmentioning

confidence: 99%

ERCC4: a potential regulatory factor in inflammatory bowel disease and inflammation-associated colorectal cancer

Shi,

Wang,

Jiang

et al. 2024

Front. Endocrinol.

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“…These non-surgical methods cause single- and double-strand DNA breaks, either directly or indirectly, which result in tumor cytotoxicity [ 1 ]. As part of the DNA damage response (DDR), the cell responds by recruitment of an assortment of proteins and enzymes, amongst other role players, to facilitate the restoration of DNA and cellular integrity [ 2 ]. There are various methods for repairing single- or double-stranded DNA damage.…”

Section: Introductionmentioning

confidence: 99%

[18F]F-Poly(ADP-Ribose) Polymerase Inhibitor Radiotracers for Imaging PARP Expression and Their Potential Clinical Applications in Oncology

Ndlovu,

Lawal,

Mdanda

et al. 2024

JCM

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Including poly(ADP-ribose) polymerase (PARP) inhibitors in managing patients with inoperable tumors has significantly improved outcomes. The PARP inhibitors hamper single-strand deoxyribonucleic acid (DNA) repair by trapping poly(ADP-ribose)polymerase (PARP) at sites of DNA damage, forming a non-functional “PARP enzyme–inhibitor complex” leading to cell cytotoxicity. The effect is more pronounced in the presence of PARP upregulation and homologous recombination (HR) deficiencies such as breast cancer-associated gene (BRCA1/2). Hence, identifying HR-deficiencies by genomic analysis—for instance, BRCA1/2 used in triple-negative breast cancer—should be a part of the selection process for PARP inhibitor therapy. Published data suggest BRCA1/2 germline mutations do not consistently predict favorable responses to PARP inhibitors, suggesting that other factors beyond tumor mutation status may be at play. A variety of factors, including tumor heterogeneity in PARP expression and intrinsic and/or acquired resistance to PARP inhibitors, may be contributing factors. This justifies the use of an additional tool for appropriate patient selection, which is noninvasive, and capable of assessing whole-body in vivo PARP expression and evaluating PARP inhibitor pharmacokinetics as complementary to the currently available BRCA1/2 analysis. In this review, we discuss [18F]Fluorine PARP inhibitor radiotracers and their potential in the imaging of PARP expression and PARP inhibitor pharmacokinetics. To provide context we also briefly discuss possible causes of PARP inhibitor resistance or ineffectiveness. The discussion focuses on TNBC, which is a tumor type where PARP inhibitors are used as part of the standard-of-care treatment strategy.

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DNA Repair and Immune Response: Editorial

Oksenych

2022

Biomolecules

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DNA Damage Response

Abstract: DNA in our cells is constantly modified by internal and external factors [...]

Cited by 3 publications

References 23 publications

ERCC4: a potential regulatory factor in inflammatory bowel disease and inflammation-associated colorectal cancer

ERCC4: a potential regulatory factor in inflammatory bowel disease and inflammation-associated colorectal cancer

[18F]F-Poly(ADP-Ribose) Polymerase Inhibitor Radiotracers for Imaging PARP Expression and Their Potential Clinical Applications in Oncology

DNA Repair and Immune Response: Editorial

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