Evidence map›Paper›PMID 26133775›Full record

ReviewClinical cancer research : an official journal of the American Association for Cancer Research2015

Molecular Pathways: Overcoming Radiation Resistance by Targeting DNA Damage Response Pathways.

Meredith A Morgan, Theodore S Lawrence

Abstract readReview
In one paragraph

Review in Clinical cancer research : an official journal of the American Association for Cancer Research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 157 papers.

0numbers the graph read from it
0cells of the map it votes in
157citing papers in PubMed
–field-weighted citation impact
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

157 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
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  6. Review
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  8. Review
  9. Two faces of Amitriptyline in anMolecular and clinical oncology · 2026
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. TheCancer management and research · 2026
    Review
  16. Article
  17. [Mechanistic research progress on radiotherapy resistance of cancer stem cells].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025
    Review
  18. Article
  19. Article
  20. Review

97 more citing papers are in PubMed but not listed here.

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

2 authors.

Meredith A MorganDepartment of Radiation Oncology, University of Michigan Medical School, Ann Arbor, Michigan. mmccrack@med.umich.edu.
Theodore S LawrenceDepartment of Radiation Oncology, University of Michigan Medical School, Ann Arbor, Michigan.

Funding

Translational Research in GI CancerP50CA130810 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BRENNER, DEAN E. · 2010 to 2016
$11.8M
Mechanism-Based Use of Chk1 Inhibitors in Pancreas CancerR01CA138723 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LAWRENCE, THEODORE S, MAYBAUM, JONATHAN · 2010 to 2015
$2.0M
Selective Sensitization of Pancreatic Cancer to Therapy by Chk1 and PARP1 InhibitR01CA163895 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MORGAN, MEREDITH A · 2012 to 2016
$1.6M
Investigating DNA repair vulnerabilities in oncometabolite producing cancersF31CA260794 · NCI · YALE UNIVERSITY · PI NORONHA, KATELYN · 2021 to 2023
$122k
NCI NIH HHS F31 CA260794NCI NIH HHS P3CA130810NCI NIH HHS P50 CA130810NCI NIH HHS P50CA130810NCI NIH HHS R01 CA138723NCI NIH HHS R01CA138723NCI NIH HHS R01 CA163895NCI NIH HHS R01CA163895
6 · The paper itself

Abstract

DNA double-strand breaks are the critical lesions responsible for the majority of ionizing radiation-induced cell killing. Thus, the ability of tumor cells to elicit a DNA damage response following radiation, via activation of DNA repair and cell-cycle checkpoints, promotes radiation resistance and tumor cell survival. Consequently, agents that target these DNA damage response pathways are being developed to overcome radiation resistance. Overall, these agents are effective radiosensitizers; however, their mechanisms of tumor cell selectivity are not fully elucidated. In this review, we focus on the crucial radiation-induced DNA damage responses as well as clinical and translational advances with agents designed to inhibit these responses. Importantly, we describe how synthetic lethality can provide tumor cell-selective radiosensitization by these agents and expand the therapeutic window for DNA damage response-targeted agents used in combination with radiotherapy.

Indexed as

DNA DamageDNA RepairHumansMolecular Targeted TherapyNeoplasmsRadiation-Sensitizing AgentsRadiation ToleranceRadiation-Sensitizing Agents

Identifiers

PMID26133775
PMCPMC4494107

What OpenQuestion holds

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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.