Evidence map›Paper›PMID 26791779›Full record

ArticleMolecular oncology2016

Hypoxia-induced alterations of G2 checkpoint regulators.

Grete Hasvold, Christin Lund-Andersen, Malin Lando, Sebastian Patzke, Sissel Hauge, ZhenHe Suo, Heidi Lyng, Randi G Syljuåsen

Open access · bronzeAbstract read
In one paragraph

Article in Molecular oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

17 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Hypoxic adaptation theory of cancer.Frontiers in cell and developmental biology · 2026
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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

8 authors at 1 institution in 1 country.

Grete HasvoldDepartment of Radiation Biology, Institute for Cancer Research, Oslo University Hospital, 0310 Oslo, Norway.
Christin Lund-AndersenDepartment of Radiation Biology, Institute for Cancer Research, Oslo University Hospital, 0310 Oslo, Norway.
Malin LandoDepartment of Radiation Biology, Institute for Cancer Research, Oslo University Hospital, 0310 Oslo, Norway.
Sebastian PatzkeDepartment of Radiation Biology, Institute for Cancer Research, Oslo University Hospital, 0310 Oslo, Norway.
Sissel HaugeDepartment of Radiation Biology, Institute for Cancer Research, Oslo University Hospital, 0310 Oslo, Norway.
ZhenHe SuoDepartment of Pathology, Norwegian Radium Hospital, Oslo University Hospital, 0310 Oslo, Norway; Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway.
Heidi LyngDepartment of Radiation Biology, Institute for Cancer Research, Oslo University Hospital, 0310 Oslo, Norway.
Randi G SyljuåsenDepartment of Radiation Biology, Institute for Cancer Research, Oslo University Hospital, 0310 Oslo, Norway. Electronic address: randi.syljuasen@rr-research.no.
Oslo University Hospital · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypoxia promotes an aggressive tumor phenotype with increased genomic instability, partially due to downregulation of DNA repair pathways. However, genome stability is also surveilled by cell cycle checkpoints. An important issue is therefore whether hypoxia also can influence the DNA damage-induced cell cycle checkpoints. Here, we show that hypoxia (24 h 0.2% O2) alters the expression of several G2 checkpoint regulators, as examined by microarray gene expression analysis and immunoblotting of U2OS cells. While some of the changes reflected hypoxia-induced inhibition of cell cycle progression, the levels of several G2 checkpoint regulators, in particular Cyclin B, were reduced in G2 phase cells after hypoxic exposure, as shown by flow cytometric barcoding analysis of individual cells. These effects were accompanied by decreased phosphorylation of a Cyclin dependent kinase (CDK) target in G2 phase cells after hypoxia, suggesting decreased CDK activity. Furthermore, cells pre-exposed to hypoxia showed increased G2 checkpoint arrest upon treatment with ionizing radiation. Similar results were found following other hypoxic conditions (∼0.03% O2 20 h and 0.2% O2 72 h). These results demonstrate that the DNA damage-induced G2 checkpoint can be altered as a consequence of hypoxia, and we propose that such alterations may influence the genome stability of hypoxic tumors.

Indexed as

G2 Phase Cell Cycle CheckpointsCell Line, TumorDNA DamageG2 PhaseGene Expression Regulation, NeoplasticGenomic InstabilityHumansHypoxiaNeoplasmsDNA damageG2 checkpointGenome stabilityHypoxiaIonizing radiation

Identifiers

PMID26791779
PMCPMC5423158
OpenAlexW2235214586

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.