Evidence map›Paper›PMID 29953367›Full record

ReviewCritical reviews in oncogenesis2018

Profiles of Radioresistance Mechanisms in Prostate Cancer.

Luksana Chaiswing, Heidi L Weiss, Rani D Jayswal, Daret K St Clair, Natasha Kyprianou

Open access · greenAbstract readReview
In one paragraph

Review in Critical reviews in oncogenesis, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

46 citing papers in PubMed, 80 citations in OpenAlex.

  1. Article
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  5. Review
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  8. KEAP1-mutant atypical meningioma: illustrative case.Journal of neurosurgery. Case lessons · 2024
    Article
  9. Review
  10. Review
  11. DNA repair in tumor radioresistance: insights from fruit flies genetics.Cellular oncology (Dordrecht, Netherlands) · 2024
    Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
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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 at 2 institutions in 1 country.

Luksana ChaiswingDepartment of Toxicology and Cancer Biology, University of Kentucky, Lexington, Kentucky.
Heidi L WeissThe Markey Biostatistics and Bioinformatics Shared Resource Facility, University of Kentucky, Lexington, Kentucky.
Rani D JayswalThe Markey Biostatistics and Bioinformatics Shared Resource Facility, University of Kentucky, Lexington, Kentucky.
Daret K St ClairDepartment of Toxicology and Cancer Biology, University of Kentucky, Lexington, Kentucky.
Natasha KyprianouDepartment of Toxicology and Cancer Biology, Department of Urology, Department of Biochemistry, University of Kentucky, Lexington, Kentucky.
University of Kentucky · USMarkey Cancer Center · US

Funding

University of Kentucky Center for Cancer MetabolismP20GM121327 · NIGMS · UNIVERSITY OF KENTUCKY · PI Jianhang Jia · 2017 to 2026
$25.0M
Distinct Redox Mechanism in Normal and Cancer Cells as a Novel Therapeutic TargetR01CA205400 · NCI · UNIVERSITY OF KENTUCKY · PI ST CLAIR, DARET K, ST CLAIR, WILLIAM H · 2016 to 2020
$1.7M
Oxidized redox state, a new potential biomarker for prostate cancer progressionR21CA188792 · NCI · UNIVERSITY OF KENTUCKY · PI CHAISWING, LUKSANA · 2015 to 2016
$371k
NCI NIH HHS R01 CA205400NCI NIH HHS R21 CA188792NIGMS NIH HHS P20 GM121327
6 · The paper itself

Abstract

Radiation therapy (RT) is commonly used for the treatment of localized prostate cancer (PCa). However, cancer cells often develop resistance to radiation through unknown mechanisms and pose an intractable challenge. Radiation resistance is highly unpredictable, rendering the treatment less effective in many patients and frequently causing metastasis and cancer recurrence. Understanding the molecular events that cause radioresistance in PCa will enable us to develop adjuvant treatments for enhancing the efficacy of RT. Radioresistant PCa depends on the elevated DNA repair system and the intracellular levels of reactive oxygen species (ROS) to proliferate, self-renew, and scavenge anti-cancer regimens, whereas the elevated heat shock protein 90 (HSP90) and the epithelial-mesenchymal transition (EMT) enable radioresistant PCa cells to metastasize after exposure to radiation. The up-regulation of the DNA repairing system, ROS, HSP90, and EMT effectors has been studied extensively, but not targeted by adjuvant therapy of radioresistant PCa. Here, we emphasize the effects of ionizing radiation and the mechanisms driving the emergence of radioresistant PCa. We also address the markers of radioresistance, the gene signatures for the predictive response to radiotherapy, and novel therapeutic platforms for targeting radioresistant PCa. This review provides significant insights into enhancing the current knowledge and the understanding toward optimization of these markers for the treatment of radioresistant PCa.

Indexed as

BiomarkersDNA DamageEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHSP90 Heat-Shock ProteinsHumansMaleOxidation-ReductionOxidative StressProstatic NeoplasmsRadiation ToleranceRadiotherapySignal TransductionTranscription FactorsBiomarkersHSP90 Heat-Shock ProteinsTranscription Factors

Identifiers

PMID29953367
PMCPMC6231577
OpenAlexW2796764897

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.