Evidence map›Paper›PMID 15034549›Full record

ArticleOncogene2004

Molecular ordering of hypoxia-induced apoptosis: critical involvement of the mitochondrial death pathway in a FADD/caspase-8 independent manner.

Martin Weinmann, Verena Jendrossek, Rene Handrick, Dilek Güner, Barbara Goecke, Claus Belka

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

23 citing papers in PubMed, 62 citations in OpenAlex.

  1. Review
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  12. Oxidative stress, unfolded protein response, and apoptosis in developmental toxicity.International review of cell and molecular biology · 2015
    Review
  13. Review
  14. Review
  15. Article
  16. Review
  17. Hypoxia alters MicroRNA expression in rat cortical pericytes.MicroRNA (Shariqah, United Arab Emirates) · 2013
    Article
  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

6 authors at 2 institutions in 1 country.

Martin WeinmannDepartment of Radiation Oncology, University of Tübingen, Germany.
Verena Jendrossek
Rene Handrick
Dilek Güner
Barbara Goecke
Claus Belka
University of Tübingen · DECharité - Universitätsmedizin Berlin · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dys-regulated growth and improper angiogenesis commonly lead to areas of hypoxia in human tumors. Hypoxia is known to be associated with a worse outcome since a lack of oxygen interferes with the efficacy of chemotherapy or radiotherapy. In parallel, hypoxia-induced apoptosis may also impose a selection pressure favoring growth of more resistant tumor cells. However, the mechanisms of hypoxia-induced apoptosis and the relative contribution of intrinsic and extrinsic apoptotic pathways are not understood. Therefore, Jurkat cell lines with defined defects in the extrinsic or intrinsic signaling cascades were used to evaluate the role of either pathway for induction of apoptosis under hypoxic conditions. Jurkat cells were incubated in hypoxia and the rate of apoptosis induction was determined by Western blotting, fluorescence microscopy and flow cytometry. Hypoxia-induced apoptosis was not affected by lack of caspase-8 or FADD, whereas overexpression of Bcl-2 or expression of dominant-negative caspase-9 mutant rendered the cells resistant to hypoxia-induced apoptosis. These results suggest that hypoxia-induced apoptosis mainly relies on intrinsic, mitochondrial pathways, whereas extrinsic pathways have no significant implications in this process. Thus, in human tumors, hypoxia will mainly lead to the selection of hypoxia-resistant cells with defects in mitochondrial apoptosis signaling pathways.

Indexed as

Adaptor Proteins, Signal TransducingApoptosisCell HypoxiaTranscription FactorsCarrier ProteinsCaspase 8Caspase 9CaspasesDNA-Binding ProteinsFas-Associated Death Domain ProteinHumansHypoxia-Inducible Factor 1Hypoxia-Inducible Factor 1, alpha SubunitJurkat CellsMitochondriaNuclear ProteinsAdaptor Proteins, Signal TransducingCarrier ProteinsCASP8 protein, humanCASP9 protein, humanCaspase 8Caspase 9CaspasesDNA-Binding ProteinsFADD protein, humanFas-Associated Death Domain ProteinHIF1A protein, humanHypoxia-Inducible Factor 1Hypoxia-Inducible Factor 1, alpha SubunitNuclear ProteinsPoly(ADP-ribose) PolymerasesTranscription FactorsTumor Suppressor Protein p53

Identifiers

PMID15034549
OpenAlexW1996400767

What OpenQuestion holds

Textmetadata
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.