Evidence map›Paper›PMID 32462882›Full record

ReviewThe British journal of radiology2020

Emerging strategies to target cancer metabolism and improve radiation therapy outcomes.

Martin Kery, Ioanna Papandreou

Open access · greenAbstract readReview
In one paragraph

Review in The British journal of radiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.0field-weighted citation impact, top 27% 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

23 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Article
  3. Membrane Stress and Ferroptosis: Lipid Dynamics in Cancer.International journal of molecular sciences · 2026
    Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Give and Take: The Reciprocal Control of Metabolism and Cell Cycle.Methods in molecular biology (Clifton, N.J.) · 2024
    Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Review
  18. Targeting the methionine addiction of cancer.American journal of cancer research · 2022
    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

2 authors at 1 institution in 1 country.

Martin Kery
Ioanna PapandreouDepartment of Radiation Oncology, Wexner Medical Center and Comprehensive Cancer Center The Ohio State University Columbus, OH, USA.
The Ohio State University Wexner Medical Center · US

Funding

HILPDA and lipid metabolism in colorectal cancerR03CA191653 · NCI · OHIO STATE UNIVERSITY · PI PAPANDREOU, IOANNA · 2015 to 2016
$154k
NCI NIH HHS R03 CA191653
6 · The paper itself

Abstract

Cancer-specific metabolic changes support the anabolic needs of the rapidly growing tumor, maintain a favorable redox balance, and help cells adapt to microenvironmental stresses like hypoxia and nutrient deprivation. Radiation is extensively applied in a large number of cancer treatment protocols but despite its curative potential, radiation resistance and treatment failures pose a serious problem. Metabolic control of DNA integrity and genomic stability can occur through multiple processes, encompassing cell cycle regulation, nucleotide synthesis, epigenetic regulation of gene activity, and antioxidant defenses. Given the important role of metabolic pathways in oxidative damage responses, it is necessary to assess the potential for tumor-specific radiosensitization by novel metabolism-targeted therapies. Additionally, there are opportunities to identify molecular and functional biomarkers of vulnerabilities to combination treatments, which could then inform clinical decisions. Here, we present a curated list of metabolic pathways in the context of ionizing radiation responses. Glutamine metabolism influences DNA damage responses by mechanisms such as synthesis of nucleotides for DNA repair or of glutathione for ROS detoxification. Repurposed oxygen consumption inhibitors have shown promising radiosensitizing activity against murine model tumors and are now in clinical trials. Production of 2-hydroxy glutarate by isocitrate dehydrogenase1/2 neomorphic oncogenic mutants interferes with the function of α-ketoglutarate-dependent enzymes and modulates Ataxia Telangiectasia Mutated (ATM) signaling and glutathione pools. Radiation-induced oxidative damage to membrane phospholipids promotes ferroptotic cell loss and cooperates with immunotherapies to improve tumor control. In summary, there are opportunities to enhance the efficacy of radiotherapy by exploiting cell-inherent vulnerabilities and dynamic microenvironmental components of the tumor.

Indexed as

Adaptation, PhysiologicalAnimalsAtaxia Telangiectasia Mutated ProteinsDNADNA DamageDNA RepairGenomic InstabilityGlutamineGlutaratesGlutathioneHumansImmunotherapyIsocitrate DehydrogenaseKetoglutaric AcidsLipid PeroxidationMicealpha-hydroxyglutarateAtaxia Telangiectasia Mutated ProteinsATM protein, humanDNAGlutamineGlutaratesGlutathioneIDH2 protein, humanIsocitrate DehydrogenaseKetoglutaric AcidsNucleotidesPhospholipidsRadiation-Sensitizing AgentsReactive Oxygen Species

Identifiers

PMID32462882
PMCPMC8519637
OpenAlexW3032256957

What OpenQuestion holds

Textmetadata
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.