Evidence map›Paper›PMID 28869494›Full record

ReviewInternational journal of molecular sciences2017

"Dicing and Splicing" Sphingosine Kinase and Relevance to Cancer.

Nahal Haddadi, Yiguang Lin, Ann M Simpson, Najah T Nassif, Eileen M McGowan

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

24 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Article
  3. A role for plasma membrane CaPflugers Archiv : European journal of physiology · 2024
    Article
  4. Article
  5. Article
  6. Review
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  11. Review
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  15. Review
  16. Article
  17. Article
  18. Article
  19. Molecular mechanisms of regulation of sphingosine kinase 1.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2018
    Review
  20. The Enigma of Sphingolipids in Health and Disease.International journal of molecular sciences · 2018
    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

5 authors at 1 institution in 1 country.

Nahal HaddadiSchool of Life Sciences, Faculty of Science, University of Technology Sydney, 15 Broadway, Ultimo, Sydney, NSW 2007, Australia. Nahal.Haddadi@student.uts.edu.au.
Yiguang LinSchool of Life Sciences, Faculty of Science, University of Technology Sydney, 15 Broadway, Ultimo, Sydney, NSW 2007, Australia. Yiguang.Lin@uts.edu.au.
Ann M SimpsonSchool of Life Sciences, Faculty of Science, University of Technology Sydney, 15 Broadway, Ultimo, Sydney, NSW 2007, Australia. Ann.Simpson@uts.edu.au.
Najah T NassifSchool of Life Sciences, Faculty of Science, University of Technology Sydney, 15 Broadway, Ultimo, Sydney, NSW 2007, Australia. Najah.Nassif@uts.edu.au.
Eileen M McGowanSchool of Life Sciences, Faculty of Science, University of Technology Sydney, 15 Broadway, Ultimo, Sydney, NSW 2007, Australia. Eileen.McGowan@uts.edu.au.
University of Technology Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sphingosine kinase (SphK) is a lipid enzyme that maintains cellular lipid homeostasis. Two SphK isozymes, SphK1 and SphK2, are expressed from different chromosomes and several variant isoforms are expressed from each of the isozymes, allowing for the multi-faceted biological diversity of SphK activity. Historically, SphK1 is mainly associated with oncogenicity, however in reality, both SphK1 and SphK2 isozymes possess oncogenic properties and are recognized therapeutic targets. The absence of mutations of SphK in various cancer types has led to the theory that cancer cells develop a dependency on SphK signaling (hyper-SphK signaling) or "non-oncogenic addiction". Here we discuss additional theories of SphK cellular mislocation and aberrant "dicing and splicing" as contributors to cancer cell biology and as key determinants of the success or failure of SphK/S1P (sphingosine 1 phosphate) based therapeutics.

Indexed as

Gene Expression Regulation, NeoplasticMultigene FamilyRNA SplicingAnimalsDisease Models, AnimalEvolution, MolecularHumansIsoenzymesLysophospholipidsNeoplasmsPhosphotransferases (Alcohol Group Acceptor)Protein TransportReceptors, LysosphingolipidSignal TransductionSphingosineSphingosine KinaseIsoenzymesLysophospholipidsPhosphotransferases (Alcohol Group Acceptor)Receptors, LysosphingolipidSphingosinesphingosine 1-phosphateSphingosine Kinasecancer therapyisozymessphingosine 1 phosphate (S1P)sphingosine kinase (SphK)variant isoforms

Identifiers

PMID28869494
PMCPMC5618540
OpenAlexW2752884184

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.