Evidence map›Paper›PMID 27518436›Full record

ArticleCell death and differentiation2016

Caspase-2 deficiency accelerates chemically induced liver cancer in mice.

S Shalini, A Nikolic, C H Wilson, J Puccini, N Sladojevic, J Finnie, L Dorstyn, S Kumar

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2016. 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
2.8field-weighted citation impact, top 9% 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, 43 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Diethylnitrosamine Induction of Hepatocarcinogenesis in Mice.Methods in molecular biology (Clifton, N.J.) · 2024
    Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Targeting apoptotic caspases in cancer.Biochimica et biophysica acta. Molecular cell research · 2020
    Review
  14. Caspase-2 Substrates: To Apoptosis, Cell Cycle Control, and Beyond.Frontiers in cell and developmental biology · 2020
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  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

8 authors at 3 institutions in 1 country.

S ShaliniCentre for Cancer Biology, University of South Australia, Adelaide, SA 5000, Australia.
A NikolicCentre for Cancer Biology, University of South Australia, Adelaide, SA 5000, Australia.
C H WilsonCentre for Cancer Biology, University of South Australia, Adelaide, SA 5000, Australia.
J PucciniCentre for Cancer Biology, University of South Australia, Adelaide, SA 5000, Australia.
N SladojevicCentre for Cancer Biology, University of South Australia, Adelaide, SA 5000, Australia.
J FinnieSA Pathology and School of Medical and Veterinary Science, University of Adelaide, Adelaide, SA 5000, Australia.
L DorstynCentre for Cancer Biology, University of South Australia, Adelaide, SA 5000, Australia.
S KumarCentre for Cancer Biology, University of South Australia, Adelaide, SA 5000, Australia.
Centre for Cancer Biology · AUUniversity of South Australia · AUUniversity of Adelaide · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aberrant cell death/survival has a critical role in the development of hepatocellular carcinoma (HCC). Caspase-2, a cell death protease, limits oxidative stress and chromosomal instability. To study its role in reactive oxygen species (ROS) and DNA damage-induced liver cancer, we assessed diethylnitrosamine (DEN)-mediated tumour development in caspase-2-deficient (Casp2(-/-)) mice. Following DEN injection in young animals, tumour development was monitored for 10 months. We found that DEN-treated Casp2(-/-) mice have dramatically elevated tumour burden and accelerated tumour progression with increased incidence of HCC, accompanied by higher oxidative damage and inflammation. Furthermore, following acute DEN injection, liver injury, DNA damage, inflammatory cytokine release and hepatocyte proliferation were enhanced in mice lacking caspase-2. Our study demonstrates for the first time that caspase-2 limits the progression of tumourigenesis induced by an ROS producing and DNA damaging reagent. Our findings suggest that after initial DEN-induced DNA damage, caspase-2 may remove aberrant cells to limit liver damage and disease progression. We propose that Casp2(-/-) mice, which are more susceptible to genomic instability, are limited in their ability to respond to DNA damage and thus carry more damaged cells resulting in accelerated tumourigenesis.

Indexed as

AnimalsCarcinoma, HepatocellularCaspase 2Cell DeathCell ProliferationDiethylnitrosamineDNA DamageEnzyme ActivationInflammationJNK Mitogen-Activated Protein KinasesLiverLiver NeoplasmsMaleMice, Inbred C57BLNeoplasm StagingOxidative StressCaspase 2DiethylnitrosamineJNK Mitogen-Activated Protein Kinases

Identifiers

PMID27518436
PMCPMC5041200
OpenAlexW2511450692

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.