Evidence map›Paper›PMID 26075267›Full record

ArticleBioMed research international2015

Cosuppression of Sprouty and Sprouty-related negative regulators of FGF signalling in prostate cancer: a working hypothesis.

Stephen J Assinder, Daniella Beniamen, Frank J Lovicu

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.5field-weighted citation impact, top 35% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Progress in experimental research on SPRED protein family.The Journal of international medical research · 2020
    Review
  2. Aging · 2020
    Article
  3. Review
  4. Article
  5. 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

3 authors at 1 institution in 1 country.

Stephen J AssinderDisciplines of Physiology, School of Medical Sciences and Bosch Institute, University of Sydney, Sydney, NSW 2006, Australia.
Daniella BeniamenDisciplines of Physiology, School of Medical Sciences and Bosch Institute, University of Sydney, Sydney, NSW 2006, Australia.
Frank J LovicuAnatomy and Histology, School of Medical Sciences and Bosch Institute, University of Sydney, Sydney, NSW 2006, Australia.
University of Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Deregulation of FGF receptor tyrosine kinase (RTK) signalling is common in prostate cancer. Normally, to moderate RTK signalling, induction of Sprouty (SPRY) and Sprouty-related (SPRED) antagonists occurs. Whilst decreased SPRY and SPRED has been described in some cancers, their role in prostate cancer is poorly understood. Therefore, we hypothesise that due to the need for tight regulation of RTK signalling, SPRY and SPRED negative regulators provide a degree of redundancy which ensures that a suppression of one or more family member does not lead to disease. Contrary to this, our analyses of prostates from 24-week-old Spry1- or Spry2-deficientmice, either hemizygous (+/-) or homozygous (-/-) for the null allele, revealed a significantly greater incidence of PIN compared to wild-type littermates. We further investigated redundancy of negative regulators in the clinical setting in a preliminary analysis of Gene Expression Omnibus and Oncomine human prostate cancer datasets. Consistent with our hypothesis, in two datasets analysed a significant cosuppression of SPRYs and SPREDs is evident. These findings demonstrate the importance of negative regulators of receptor tyrosine signalling, such as Spry, in the clinical setting, and highlight their importance for future pharmacopeia.

Indexed as

Signal TransductionAdaptor Proteins, Signal TransducingAnimalsFibroblast Growth FactorsHumansIntracellular Signaling Peptides and ProteinsMaleMembrane ProteinsMiceMice, KnockoutNeoplasm ProteinsPhosphoproteinsProstatic NeoplasmsProtein Serine-Threonine KinasesRepressor ProteinsAdaptor Proteins, Signal TransducingFibroblast Growth FactorsIntracellular Signaling Peptides and ProteinsMembrane ProteinsNeoplasm ProteinsPhosphoproteinsProtein Serine-Threonine KinasesRepressor ProteinsSPRED1 protein, humanSpred1 protein, mouseSPRED2 protein, humanSpred2 protein, mouseSPRY1 protein, humanSpry1 protein, mouseSPRY2 protein, humanSpry2 protein, mouse

Identifiers

PMID26075267
PMCPMC4449890
OpenAlexW1588380777

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.