Evidence map›Paper›PMID 22419115›Full record

ArticleCell death & disease2012

Re-oxygenation causes hypoxic tumor regression through restoration of p53 wild-type conformation and post-translational modifications.

R Gogna, E Madan, P Kuppusamy, U Pati

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

25 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. HIF-transcribed p53 chaperones HIF-1α.Nucleic acids research · 2019
    Article
  9. Article
  10. Article
  11. Altered p53 functionality in cancer-associated fibroblasts contributes to their cancer-supporting features.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  12. Article
  13. p53 shades of Hippo.Cell death and differentiation · 2018
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. 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

4 authors at 2 institutions in 2 countries.

R GognaTranscription and Human Biology Laboratory, School of Biotechnology, Jawaharlal Nehru University, New Delhi, India.
E Madan
P Kuppusamy
U Pati
Jawaharlal Nehru University · INLung Institute · US

Funding

Probes and Methods for Clinical OximetryR01EB004031 · NIBIB · OHIO STATE UNIVERSITY · PI KUPPUSAMY, PERIANNAN · 2004 to 2021
$7.1M
NIBIB NIH HHS EB004031NIBIB NIH HHS R01 EB004031
6 · The paper itself

Abstract

Hypoxic tumors are resistant to conventional therapies through indirect mechanisms such as the selection of resistant phenotype under chronic hypoxia. Hyperbaric oxygen (HBO) therapy has been shown to increase oxygen level and induce apoptosis in hypoxic tumor. However, it could produce significant adverse effects including oxygen toxic seizures and severe radiation tissue injury due to high pressure. We have shown that repeated oxygenation at 30% O(2) (1 atmospheres absolute) results in significant regression of MCF-7 tumor xenografts without any adverse effect. In MCF-7 cells, re-oxygenation showed an eightfold increase in cellular apoptosis. Both in hypoxic tumor and in hypoxic cells, that exclusively favor p53 to exist in mutant conformation, re-oxygenation restores p53 wild-type conformation. The oxygen-mediated rescue of mutant p53 followed by its trans-activation is responsible for the induction of p53-downstream apoptotic, cell-cycle arrest and DNA-repair genes. Further, p53 trans-activation may thus be due to its post-translational modifications as a result of re-oxygenation. We have thus concluded that oxygen therapy without pressure, as opposed to HBO therapy, may be ideal for hypoxic tumor regression, which functions through oxygen-mediated rescue of mutant p53 followed by induction of apoptosis.

Indexed as

AcetylationAnimalsApoptosisCell HypoxiaCell Line, TumorGenes, ReporterHumansLuciferasesMiceMice, NudeNeoplasms, ExperimentalOxygenPhosphorylationPlasmidsProtein ConformationProtein Processing, Post-TranslationalLuciferasesOxygenTumor Suppressor Protein p53

Identifiers

PMID22419115
PMCPMC3317354
OpenAlexW2015584395

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.