Evidence map›Paper›PMID 24411622›Full record

ArticleInternational journal of radiation oncology, biology, physics2014

Acquired tumor cell radiation resistance at the treatment site is mediated through radiation-orchestrated intercellular communication.

Natarajan Aravindan, Sheeja Aravindan, Vijayabaskar Pandian, Faizan H Khan, Satish Kumar Ramraj, Praveen Natt, Mohan Natarajan

Abstract read
In one paragraph

Article in International journal of radiation oncology, biology, physics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

20 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Low-Dose Non-Targeted Effects and Mitochondrial Control.International journal of molecular sciences · 2023
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. SUMOylation and phosphorylation cross-talk in hepatocellular carcinoma.Translational gastroenterology and hepatology · 2018
    Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Ionizing radiation: mechanisms and therapeutics.Antioxidants & redox signaling · 2014
    Article
  19. Biological response of cancer cells to radiation treatment.Frontiers in molecular biosciences · 2014
    Review
  20. Article
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

7 authors at 2 institutions in 1 country.

Natarajan AravindanDepartment of Radiation Oncology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma. Electronic address: naravind@ouhsc.edu.
Sheeja AravindanDepartment of Radiation Oncology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma.
Vijayabaskar PandianDepartment of Radiation Oncology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma.
Faizan H KhanDepartment of Radiation Oncology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma.
Satish Kumar RamrajDepartment of Radiation Oncology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma.
Praveen NattDepartment of Radiation Oncology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma.
Mohan NatarajanDepartment of Pathology, The University of Texas Health Science Center at San Antonio, San Antonio, Texas.
University of Oklahoma Health Sciences Center · USThe University of Texas Health Science Center at San Antonio · US

Funding

TUMOR RESISTANCE MECHANISMS TO ANTI-VEGF THERAPY IN PROSTATE CANCER (Sukyung Woo)P20GM103639 · NIGMS · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI HANNAFON, BETHANY · 2012 to 2022
$21.3M
ENHANCED APOPTOSIS BY TARGETING PROTEIN REDOX STATUSR01CA112175 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI NATARAJAN, MOHAN · 2006 to 2009
$705k
NCI NIH HHS R01 CA112175NIGMS NIH HHS 1P20GM103639-01NIGMS NIH HHS P20 GM103639
6 · The paper itself

Abstract

purposeRadiation resistance induced in cancer cells that survive after radiation therapy (RT) could be associated with increased radiation protection, limiting the therapeutic benefit of radiation. Herein we investigated the sequential mechanistic molecular orchestration involved in radiation-induced radiation protection in tumor cells.

resultsRadiation, both in the low-dose irradiation (LDIR) range (10, 50, or 100 cGy) or at a higher, challenge dose IR (CDIR), 4 Gy, induced dose-dependent and sustained NFκB-DNA binding activity. However, a robust and consistent increase was seen in CDIR-induced NFκB activity, decreased DNA fragmentation, apoptosis, and cytotoxicity and attenuation of CDIR-inhibited clonal expansion when the cells were primed with LDIR prior to challenge dose. Furthermore, NFκB manipulation studies with small interfering RNA (siRNA) silencing or p50/p65 overexpression unveiled the influence of LDIR-activated NFκB in regulating CDIR-induced DNA fragmentation and apoptosis. LDIR significantly increased the transactivation/translation of the radiation-responsive factors tumor necrosis factor-α (TNF-α), interleukin-1α (IL-1α), cMYC, and SOD2. Coculture experiments exhibit LDIR-influenced radiation protection and increases in cellular expression, secretion, and activation of radiation-responsive molecules in bystander cells. Individual gene-silencing approach with siRNAs coupled with coculture studies showed the influence of LDIR-modulated TNF-α, IL-1α, cMYC, and SOD2 in induced radiation protection in bystander cells. NFκB inhibition/overexpression studies coupled with coculture experiments demonstrated that TNF-α, IL-1α, cMYC, and SOD2 are selectively regulated by LDIR-induced NFκB.

conclusionsTogether, these data strongly suggest that scattered LDIR-induced NFκB-dependent TNF-α, IL-1α, cMYC, and SOD2 mediate radiation protection to the subsequent challenge dose in tumor cells.

Indexed as

Neoplasm Recurrence, LocalScattering, RadiationApoptosisBystander EffectCell SurvivalDNA FragmentationDNA, NeoplasmHumansInterferon-alphaNeoplasm ProteinsNF-kappa BNF-kappa B p50 SubunitProto-Oncogene Proteins c-mycRadiation DosageRadiation ToleranceRNA, Small InterferingDNA, NeoplasmInterferon-alphaMYC protein, humanNeoplasm ProteinsNF-kappa BNF-kappa B p50 SubunitProto-Oncogene Proteins c-mycRNA, Small InterferingSuperoxide DismutaseSuperoxide Dismutase 2Transcription Factor RelATumor Necrosis Factor-alpha

Identifiers

PMID24411622
PMCPMC4034458
OpenAlexW2044993258

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.