Radiobiology Summaries: DNA Damage and Repair

Chalmers, Anthony J.; Carruthers, Ross

doi:10.1016/j.clon.2020.12.006

Cited by 3 publications

(3 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…XRCC1, bifunctional polynucleotide phosphatase/kinase PNK, Flap endonuclease 1 and, finally, DNA ligases I and III 15 . DSBs are broadly repaired by either non-homologous end-joining (NHEJ), which can be error prone, or high-fidelity homologous recombination repair 16 .…”

Section: Review Articlementioning

confidence: 99%

Predicting tumour radiosensitivity to deliver precision radiotherapy

2022

View full text Add to dashboard Cite

Owing to advances in radiotherapy, the physical properties of radiation can be optimized to enable individualized treatment; however, optimization is rarely based on biological properties and, therefore, treatments are generally planned with the assumption that all tumours respond similarly to radiation. Radiation affects multiple cellular pathways, including DNA damage, hypoxia, proliferation, stem cell phenotype and immune response. In this Review, we summarize the effect of these pathways on tumour responses to radiotherapy and the current state of research on genomic classifiers designed to exploit these variations to inform treatment decisions. We also discuss whether advances in genomics have generated evidence that could be practice changing and whether advances in genomics are now ready to be used

show abstract

Section: Review Articlementioning

confidence: 99%

Predicting tumour radiosensitivity to deliver precision radiotherapy

2022

View full text Add to dashboard Cite

show abstract

“…5,10 Accordingly, this process must recognize the DNA damage first to initiate the DDR signal cascade, and then this signal must be transduced to the DNA damage repair machinery and the respective molecular regulators. [10][11][12] This signaling cascade results in an increase in the concentration of DNA repair factors at the site of the damage and can also activate the cell cycle checkpoint. 5,7 This checkpoint activation reduces the activity of cyclin-dependent kinases (CDKs) and delays the next stage of the cell cycle in order to provide time for DNA repair.…”

Section: Dna Damage Repairmentioning

confidence: 99%

“…This pathway is composed of a DNA damage sensor, signal sensor, the molecular related to transportation and repair 5,10 . Accordingly, this process must recognize the DNA damage first to initiate the DDR signal cascade, and then this signal must be transduced to the DNA damage repair machinery and the respective molecular regulators 10–12 . This signaling cascade results in an increase in the concentration of DNA repair factors at the site of the damage and can also activate the cell cycle checkpoint 5,7 .…”

Section: Dna Damagementioning

confidence: 99%

The role and mechanism of long non‐coding RNAs in homologous recombination repair of radiation‐induced DNA damage

Qin

Zhang

et al. 2022

The Journal of Gene Medicine

View full text Add to dashboard Cite

DNA double-strand breaks can seriously damage the genetic information that organisms depend on for survival and reproduction. Therefore, cells require a robust DNA damage response mechanism to repair the damaged DNA. Homologous recombination (HR) allows error-free repair, which is key to maintaining genomic integrity. Long non-coding RNAs (lncRNAs) are RNA molecules that are longer than 200 nucleotides.In recent years, a number of studies have found that lncRNAs can act as regulators of gene expression and DNA damage response mechanisms, including HR repair. Moreover, they have significant effects on the occurrence, development, invasion and metastasis of tumor cells, as well as the sensitivity of tumors to radiotherapy and chemotherapy. These studies have therefore begun to expose the great potential of lncRNAs for clinical applications. In this review, we focus on the regulatory roles of lncRNAs in HR repair.

show abstract

Hyperthermia and radiotherapy: physiological basis for a synergistic effect

Righini,

Durham,

Tsoutsou

2024

Front. Oncol.

View full text Add to dashboard Cite

In cancer treatment, mild hyperthermia (HT) represents an old, but recently revived opportunity to increase the efficacy of radiotherapy (RT) without increasing side effects, thereby widening the therapeutic window. HT disrupts cellular homeostasis by acting on multiple targets, and its combination with RT produces synergistic antitumoral effects on specific pathophysiological mechanisms, associated to DNA damage and repair, hypoxia, stemness and immunostimulation. HT is furthermore associated to direct tumor cell kill, particularly in higher temperature levels. A phenomenon of temporary resistance to heat, known as thermotolerance, follows each HT session. Cancer treatment requires innovative concepts and combinations to be tested but, for a meaningful development of clinical trials, the understanding of the underlying mechanisms of the tested modalities is essential. In this mini-review, we aimed to describe the synergistic effects of the combination of HT with RT as well as the phenomena of thermal shock and thermotolerance, in order to stimulate clinicians in new, clinically relevant concepts and combinations, which become particularly relevant in the era of technological advents in both modalities but also cancer immunotherapy.

show abstract

Radiobiology Summaries: DNA Damage and Repair

Cited by 3 publications

References 17 publications

Predicting tumour radiosensitivity to deliver precision radiotherapy

Predicting tumour radiosensitivity to deliver precision radiotherapy

The role and mechanism of long non‐coding RNAs in homologous recombination repair of radiation‐induced DNA damage

Hyperthermia and radiotherapy: physiological basis for a synergistic effect

Contact Info

Product

Resources

About