Evidence map›Paper›PMID 19883367›Full record

ReviewCritical reviews in eukaryotic gene expression2009

Molecular parameters of hyperthermia for radiosensitization.

Tej K Pandita, Shruti Pandita, Sukesh R Bhaumik

Open access · greenAbstract readReview
In one paragraph

Review in Critical reviews in eukaryotic gene expression, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

21 citing papers in PubMed, 55 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Article
  5. Photodynamic therapy in oral cancer: a review of clinical studies.Medical oncology (Northwood, London, England) · 2023
    Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Enhancement of Photodynamic Cancer Therapy by Physical and Chemical Factors.Angewandte Chemie (International ed. in English) · 2019
    Review
  11. Review
  12. Article
  13. Article
  14. Gold nanoparticle hyperthermia reduces radiotherapy dose.Nanomedicine : nanotechnology, biology, and medicine · 2014
    Article
  15. Mechanisms of heat shock response in mammals.Cellular and molecular life sciences : CMLS · 2013
    Review
  16. Review
  17. Review
  18. Article
  19. Article
  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

3 authors at 2 institutions in 1 country.

Tej K PanditaDepartment of Radiation Oncology, Washington University School of Medicine, St. Louis, Missouri 63108, USA. pandita@wustl.edu
Shruti Pandita
Sukesh R Bhaumik
Southern Illinois University School of Medicine · USWashington University in St. Louis · US

Funding

CHROMATIN MODIFYING FACTORS CONTROL RADIATION RESPONSE AND GENOMIC STABILITYR01CA129537 · NCI · WASHINGTON UNIVERSITY · PI PANDITA, TEJ K · 2008 to 2018
$3.3M
Functional Characterization of the Mammalian MOF Gene ProductR01CA123232 · NCI · WASHINGTON UNIVERSITY · PI PANDITA, TEJ K · 2007 to 2011
$1.5M
NCI NIH HHS CA10445NCI NIH HHS CA123232NCI NIH HHS CA129537NCI NIH HHS R01 CA123232NCI NIH HHS R01 CA129537
6 · The paper itself

Abstract

Hyperthermia is a potent sensitizer of cell killing by ionizing radiation (IR), however, the precise mechanism of heat-induced cell death is not yet clear. Radiosensitization can be attributed to the fact that heat is a pleiotropic damaging agent, affecting multiple cell components to varying degrees by altering protein structures, thus influencing the DNA damage response. Hyperthermia alone induces several steps associated with IR signaling in cells. For example, hyperthermia enhances ATM kinase activity and increases cellular ATM autophosphorylation. This prior activation of ATM or other components of the IR-induced signaling pathway by heat interferes with the normal IR-induced signaling required for chromosomal DNA double-strand break repair, thus resulting in increased cell killing post irradiation. Hyperthermia also induces heat shock protein 70 (HSP70) synthesis and enhances telomerase activity. HSP70 expression is associated with radioresistance. Inactivation of HSP70 and telomerase increases residual DNA DSBs post IR exposure, which correlates with increased cell killing, supporting the role of HSP70 and telomerase in IR-induced DNA damage repair. Thus, hyperthermia influences several molecular parameters involved in sensitizing tumor cells to radiation and can enhance the potential of targeted radiotherapy.

Indexed as

DNA DamageGene Expression RegulationHyperthermia, InducedAnimalsAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsDNA-Binding ProteinsDNA RepairHeat-Shock ResponseHistonesHSP70 Heat-Shock ProteinsHumansNeoplasmsProtein Serine-Threonine KinasesRadiation ToleranceTelomeraseAtaxia Telangiectasia Mutated ProteinsATM protein, humanCell Cycle ProteinsDNA-Binding ProteinsH2AX protein, humanHistonesHSP70 Heat-Shock ProteinsProtein Serine-Threonine KinasesTelomeraseTERT protein, humanTumor Suppressor Proteins

Identifiers

PMID19883367
PMCPMC3097377
OpenAlexW2092627694

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.