Evidence map›Paper›PMID 23175523›Full record

ReviewMolecular cancer research : MCR2013

Radiation survivors: understanding and exploiting the phenotype following fractionated radiation therapy.

Adeola Y Makinde, Molykutty John-Aryankalayil, Sanjeewani T Palayoor, David Cerna, C Norman Coleman

Abstract readReview
In one paragraph

Review in Molecular cancer research : MCR, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing 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

26 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Radiation-induced Adaptive Response: New Potential for Cancer Treatment.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020
    Review
  5. A tumor-immune interaction model for hepatocellular carcinoma based on measured lymphocyte counts in patients undergoing radiotherapy.Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology · 2020
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Improving the Predictive Value of Preclinical Studies in Support of Radiotherapy Clinical Trials.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016
    Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Enhancing the efficacy of radiation therapy: premises, promises, and practicality.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2014
    Article
  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

5 authors.

Adeola Y MakindeNational Institutes of Health/National Cancer Institute, 9000 Rockville Pike, Bldg 10, B3B406, Bethesda, MD 20892, USA. adeola.makinde@nih.gov
Molykutty John-Aryankalayil
Sanjeewani T Palayoor
David Cerna
C Norman Coleman

Funding

Radiation-induced molecular targetsZIABC010670 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI COLEMAN, NORMAN · 2009 to 2024
$17.3M
Intramural NIH HHS Z99 CA999999NCI NIH HHS Y99 CA999999
6 · The paper itself

Abstract

Radiation oncology modalities such as intensity-modulated and image-guided radiation therapy can reduce the high dose to normal tissue and deliver a heterogeneous dose to tumors, focusing on areas deemed at highest risk for tumor persistence. Clinical radiation oncology produces daily doses ranging from 1 to 20 Gy, with tissues being exposed to 30 or more daily fractions. Hypothesizing the cells that survive fractionated radiation therapy have a substantially different phenotype than the untreated cells, which might be exploitable for targeting with molecular therapeutics or immunotherapy, three prostate cancer cell lines (PC3, DU145, and LNCaP) and normal endothelial cells were studied to understand the biology of differential effects of multifraction (MF) radiation of 0.5, 1, and/or 2 Gy fraction to 10 Gy total dose, and a single dose of 5 and 10 Gy. The resulting changes in mRNA, miRNA, and phosphoproteome were analyzed. Significant differences were observed in the MF radiation exposures including those from the 0.5 Gy MF that produces little cell killing. As expected, p53 function played a major role in response. Pathways modified by MF include immune response, DNA damage, cell-cycle arrest, TGF-β, survival, and apoptotic signal transduction. The radiation-induced stress response will set forth a unique platform for exploiting the effects of radiation therapy as "focused biology" for cancer treatment in conjunction with molecular targeted or immunologically directed therapy. Given that more normal tissue is treated, albeit to lower doses with these newer techniques, the response of the normal tissue may also influence long-term treatment outcome.

Indexed as

Cell Line, TumorDose-Response Relationship, RadiationHumansNeoplasmsRadiation ToleranceRadiotherapy, Image-GuidedSurvivors

Identifiers

PMID23175523
PMCPMC3552079

What OpenQuestion holds

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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.