Evidence map›Paper›PMID 24374687›Full record

ReviewPlastic and reconstructive surgery2014

Mechanisms of injury to normal tissue after radiotherapy: a review.

Justin R Hubenak, Qixu Zhang, Cynthia D Branch, Steven J Kronowitz

Open access · greenAbstract readReview
In one paragraph

Review in Plastic and reconstructive surgery, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed, 1 pooled it
7.1field-weighted citation impact, top 3% 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

73 citing papers in PubMed, 1 synthesis or guideline pooled it, 161 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Nuclear destabilisation - a possible genesis of cancer?Biological reviews of the Cambridge Philosophical Society · 2025
    Review
  5. Article
  6. Targeting proteostasis pathways for cancer therapy.Journal of pharmaceutical analysis · 2025
    Review
  7. Article
  8. Article
  9. Article
  10. Radioresistance Mechanisms in Head and Neck Cancer.Clinical and experimental otorhinolaryngology · 2025
    Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

13 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

4 authors at 1 institution in 1 country.

Justin R HubenakHouston, Texas From the Department of Plastic and Reconstructive Surgery, The University of Texas M. D. Anderson Cancer Center.
Qixu Zhang
Cynthia D Branch
Steven J Kronowitz
The University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
NCI NIH HHS CA016672NCI NIH HHS P30 CA016672
6 · The paper itself

Abstract

backgroundThe benefits of radiotherapy for cancer have been well documented for many years, but many patients treated with radiation develop adverse effects. This study analyzed the current research into the biological basis of radiotherapy-induced normal tissue damage.

methodsUsing the PubMed and EMBASE databases, articles on adverse effects of radiotherapy on normal tissue published from January of 2005 through May of 2012 were identified. Their abstracts were reviewed for information relevant to radiotherapy-induced DNA damage and DNA repair. Articles in the reference lists that seemed relevant were reviewed with no limitations on publication date.

resultsOf 1751 publications, 1729 were eliminated because they did not address fundamental biology or were duplicates. The 22 included articles revealed that many adverse effects are driven by chronic oxidative stress affecting the nuclear function of DNA repair mechanisms. Among normal cells undergoing replication, cells in S phase are most radioresistant because of overexpression of DNA repair enzymes, while cells in M phase are especially radiosensitive. Cancer cells exhibit increased radiosensitivity, leading to accumulation of irreparable DNA lesions and cell death. Irradiated cells have an indirect effect on the cell cycle and survival of cocultured nonirradiated cells. Method of irradiation and linear energy transfer to cancer cells versus bystander cells are shown to have an effect on cell survival.

conclusionsRadiotherapy-induced increases in reactive oxygen species in irradiated cells may signal healthy cells by increasing metabolic stress and creating DNA lesions. The side effects of radiotherapy and bystander cell signaling may have a larger impact than previously acknowledged.

Indexed as

DNA DamageDatabases, FactualHumansNeoplasmsRadiation InjuriesRadiotherapy

Identifiers

PMID24374687
PMCPMC3921068
OpenAlexW1989169469

What OpenQuestion holds

Textmetadata
LicenceTDM
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.