Evidence map›Paper›PMID 25144718›Full record

ArticleCell death & disease2014

An unexpected role for caspase-2 in neuroblastoma.

L Dorstyn, J Puccini, A Nikolic, S Shalini, C H Wilson, M D Norris, M Haber, S Kumar

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.5field-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

14 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Targeting apoptotic caspases in cancer.Biochimica et biophysica acta. Molecular cell research · 2020
    Review
  8. Caspase-2 Substrates: To Apoptosis, Cell Cycle Control, and Beyond.Frontiers in cell and developmental biology · 2020
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Old, new and emerging functions of caspases.Cell death and differentiation · 2015
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 1 country.

L Dorstyn1] Centre for Cancer Biology, University of South Australia, Adelaide, SA 5001, Australia [2] Department of Medicine, University of Adelaide, Adelaide, SA 5005, Australia.
J PucciniCentre for Cancer Biology, University of South Australia, Adelaide, SA 5001, Australia.
A NikolicCentre for Cancer Biology, University of South Australia, Adelaide, SA 5001, Australia.
S ShaliniCentre for Cancer Biology, University of South Australia, Adelaide, SA 5001, Australia.
C H WilsonCentre for Cancer Biology, University of South Australia, Adelaide, SA 5001, Australia.
M D NorrisChildren's Cancer Institute Australia for Medical Research, Lowy Cancer Research Centre, UNSW, Sydney, NSW 2052, Australia.
M HaberChildren's Cancer Institute Australia for Medical Research, Lowy Cancer Research Centre, UNSW, Sydney, NSW 2052, Australia.
S Kumar1] Centre for Cancer Biology, University of South Australia, Adelaide, SA 5001, Australia [2] Department of Medicine, University of Adelaide, Adelaide, SA 5005, Australia.
University of South Australia · AUUNSW Sydney · AUCentre for Cancer Biology · AUUniversity of Adelaide · AU

Funding

Worldwide Cancer Research 13-1015
6 · The paper itself

Abstract

Caspase-2 has been implicated in various cellular functions, including cell death by apoptosis, oxidative stress response, maintenance of genomic stability and tumor suppression. The loss of the caspase-2 gene (Casp2) enhances oncogene-mediated tumorigenesis induced by E1A/Ras in athymic nude mice, and also in the Eμ-Myc lymphoma and MMTV/c-neu mammary tumor mouse models. To further investigate the function of caspase-2 in oncogene-mediated tumorigenesis, we extended our studies in the TH-MYCN transgenic mouse model of neuroblastoma. Surprisingly, we found that loss of caspase-2 delayed tumorigenesis in the TH-MYCN neuroblastoma model. In addition, tumors from TH-MYCN/Casp2(-/-) mice were predominantly thoracic paraspinal tumors and were less vascularized compared with tumors from their TH-MYCN/Casp2(+/+) counterparts. We did not detect any differences in the expression of neuroblastoma-associated genes in TH-MYCN/Casp2(-/-) tumors, or in the activation of Ras/MAPK signaling pathway that is involved in neuroblastoma progression. Analysis of expression array data from human neuroblastoma samples showed a correlation between low caspase-2 levels and increased survival. However, caspase-2 levels correlated with clinical outcome only in the subset of MYCN-non-amplified human neuroblastoma. These observations indicate that caspase-2 is not a suppressor in MYCN-induced neuroblastoma and suggest a tissue and context-specific role for caspase-2 in tumorigenesis.

Indexed as

AnimalsCaspase 2Disease Models, AnimalHumansKaplan-Meier EstimateMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicMitogen-Activated Protein KinasesNeuroblastomaras ProteinsSignal TransductionCaspase 2Mitogen-Activated Protein Kinasesras Proteins

Identifiers

PMID25144718
PMCPMC4454317
OpenAlexW2045677722

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.