Evidence map›Paper›PMID 34337349›Full record

ArticleCancer drug resistance (Alhambra, Calif.)2021

Exploiting DNA repair pathways for tumor sensitization, mitigation of resistance, and normal tissue protection in radiotherapy.

Jac A Nickoloff, Lynn Taylor, Neelam Sharma, Takamitsu A Kato

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer drug resistance (Alhambra, Calif.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.4field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

34 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
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  8. Wogonin inhibits radiation-induced DNA damage repair in hepatocellular carcinoma cells by upregulating p21.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
    Article
  9. Article
  10. Review
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  13. Article
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  17. Crosstalk between immune checkpoint and DNA damage response inhibitors for radiosensitization of tumors.Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al] · 2023
    Review
  18. Cellular Responses to Widespread DNA Replication Stress.International journal of molecular sciences · 2023
    Review
  19. Review
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Jac A NickoloffDepartment of Environmental and Radiological Health Sciences, Colorado State University, Ft. Collins, CO 80523, USA.
Lynn TaylorDepartment of Environmental and Radiological Health Sciences, Colorado State University, Ft. Collins, CO 80523, USA.
Neelam SharmaDepartment of Environmental and Radiological Health Sciences, Colorado State University, Ft. Collins, CO 80523, USA.
Takamitsu A KatoDepartment of Environmental and Radiological Health Sciences, Colorado State University, Ft. Collins, CO 80523, USA.
Colorado State University · US

Funding

METNASE ROLES IN NHEJ, DNA INTEGRATION AND TRANSLOCATIONR01GM084020 · NIGMS · COLORADO STATE UNIVERSITY · PI NICKOLOFF, JAC A · 2009 to 2016
$2.4M
NIGMS NIH HHS R01 GM084020
6 · The paper itself

Abstract

More than half of cancer patients are treated with radiotherapy, which kills tumor cells by directly and indirectly inducing DNA damage, including cytotoxic DNA double-strand breaks (DSBs). Tumor cells respond to these threats by activating a complex signaling network termed the DNA damage response (DDR). The DDR arrests the cell cycle, upregulates DNA repair, and triggers apoptosis when damage is excessive. The DDR signaling and DNA repair pathways are fertile terrain for therapeutic intervention. This review highlights strategies to improve therapeutic gain by targeting DDR and DNA repair pathways to radiosensitize tumor cells, overcome intrinsic and acquired tumor radioresistance, and protect normal tissue. Many biological and environmental factors determine tumor and normal cell responses to ionizing radiation and genotoxic chemotherapeutics. These include cell type and cell cycle phase distribution; tissue/tumor microenvironment and oxygen levels; DNA damage load and quality; DNA repair capacity; and susceptibility to apoptosis or other active or passive cell death pathways. We provide an overview of radiobiological parameters associated with X-ray, proton, and carbon ion radiotherapy; DNA repair and DNA damage signaling pathways; and other factors that regulate tumor and normal cell responses to radiation. We then focus on recent studies exploiting DSB repair pathways to enhance radiotherapy therapeutic gain.

Indexed as

cancer therapyDNA double-strand break repairDNA repairhomologous recombinationnon-homologous end-joiningradioprotectionradiosensitization

Identifiers

PMID34337349
PMCPMC8323830
OpenAlexW3116567755

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.