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DNA Double-Strand Break Repair as Determinant of Cellular Radiosensitivity to Killing and Target in Radiation Therapy

Overview of attention for article published in Frontiers in oncology, January 2013
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219 Dimensions

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225 Mendeley
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Title
DNA Double-Strand Break Repair as Determinant of Cellular Radiosensitivity to Killing and Target in Radiation Therapy
Published in
Frontiers in oncology, January 2013
DOI 10.3389/fonc.2013.00113
Pubmed ID
Authors

Emil Mladenov, Simon Magin, Aashish Soni, George Iliakis

Abstract

Radiation therapy plays an important role in the management of a wide range of cancers. Besides innovations in the physical application of radiation dose, radiation therapy is likely to benefit from novel approaches exploiting differences in radiation response between normal and tumor cells. While ionizing radiation induces a variety of DNA lesions, including base damages and single-strand breaks, the DNA double-strand break (DSB) is widely considered as the lesion responsible not only for the aimed cell killing of tumor cells, but also for the general genomic instability that leads to the development of secondary cancers among normal cells. Homologous recombination repair (HRR), non-homologous end-joining (NHEJ), and alternative NHEJ, operating as a backup, are the major pathways utilized by cells for the processing of DSBs. Therefore, their function represents a major mechanism of radiation resistance in tumor cells. HRR is also required to overcome replication stress - a potent contributor to genomic instability that fuels cancer development. HRR and alternative NHEJ show strong cell-cycle dependency and are likely to benefit from radiation therapy mediated redistribution of tumor cells throughout the cell-cycle. Moreover, the synthetic lethality phenotype documented between HRR deficiency and PARP inhibition has opened new avenues for targeted therapies. These observations make HRR a particularly intriguing target for treatments aiming to improve the efficacy of radiation therapy. Here, we briefly describe the major pathways of DSB repair and review their possible contribution to cancer cell radioresistance. Finally, we discuss promising alternatives for targeting DSB repair to improve radiation therapy and cancer treatment.

X Demographics

X Demographics

The data shown below were collected from the profiles of 5 X users who shared this research output. Click here to find out more about how the information was compiled.
Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 225 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
United Kingdom 1 <1%
Israel 1 <1%
United States 1 <1%
Bulgaria 1 <1%
Unknown 221 98%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 46 20%
Researcher 46 20%
Student > Master 21 9%
Student > Bachelor 19 8%
Student > Doctoral Student 17 8%
Other 33 15%
Unknown 43 19%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 58 26%
Agricultural and Biological Sciences 53 24%
Medicine and Dentistry 25 11%
Chemistry 9 4%
Pharmacology, Toxicology and Pharmaceutical Science 8 4%
Other 24 11%
Unknown 48 21%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 3. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 25 December 2019.
All research outputs
#14,929,728
of 25,394,764 outputs
Outputs from Frontiers in oncology
#4,150
of 22,440 outputs
Outputs of similar age
#169,451
of 289,149 outputs
Outputs of similar age from Frontiers in oncology
#80
of 328 outputs
Altmetric has tracked 25,394,764 research outputs across all sources so far. This one is in the 40th percentile – i.e., 40% of other outputs scored the same or lower than it.
So far Altmetric has tracked 22,440 research outputs from this source. They receive a mean Attention Score of 3.0. This one has done well, scoring higher than 80% of its peers.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 289,149 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 40th percentile – i.e., 40% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 328 others from the same source and published within six weeks on either side of this one. This one has gotten more attention than average, scoring higher than 73% of its contemporaries.