Evidence map›Paper›PMID 36964408›Full record

ReviewNature reviews. Urology2023

Calcium signalling pathways in prostate cancer initiation and progression.

Roberto Silvestri, Vanessa Nicolì, Priyadarsini Gangadharannambiar, Francesco Crea, Martin D Bootman

Open access · greenAbstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Urology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
11.6field-weighted citation impact, top 1% 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

21 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
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  5. [Force-regulation mechanism of E-selectin mediated adhesion and activation of MDA-MB-231 cells under fluid shear stress].Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi · 2026
    Article
  6. Review
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  10. Article
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  13. Calcium channels as pharmacological targets for cancer therapy.Clinical and experimental medicine · 2025
    Review
  14. Article
  15. Article
  16. Article
  17. CaBiophysics reports · 2024
    Article
  18. Review
  19. Review
  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

5 authors at 2 institutions in 2 countries.

Roberto Silvestri *Department of Biology, University of Pisa, Pisa, Italy.ORCID 0000-0002-5588-5235
Vanessa Nicolì *Department of Translational Research and of New Surgical and Medical Technologies, University of Pisa, Pisa, Italy.
Priyadarsini GangadharannambiarCancer Research Group, School of Life Health and Chemical Sciences, The Open University, Milton Keynes, UK.
Francesco CreaCancer Research Group, School of Life Health and Chemical Sciences, The Open University, Milton Keynes, UK.
Martin D BootmanCancer Research Group, School of Life Health and Chemical Sciences, The Open University, Milton Keynes, UK. martin.bootman@open.ac.uk.ORCID 0000-0002-6447-3451
The Open University · GBUniversity of Pisa · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer cells proliferate, differentiate and migrate by repurposing physiological signalling mechanisms. In particular, altered calcium signalling is emerging as one of the most widespread adaptations in cancer cells. Remodelling of calcium signalling promotes the development of several malignancies, including prostate cancer. Gene expression data from in vitro, in vivo and bioinformatics studies using patient samples and xenografts have shown considerable changes in the expression of various components of the calcium signalling toolkit during the development of prostate cancer. Moreover, preclinical and clinical evidence suggests that altered calcium signalling is a crucial component of the molecular re-programming that drives prostate cancer progression. Evidence points to calcium signalling re-modelling, commonly involving crosstalk between calcium and other cellular signalling pathways, underpinning the onset and temporal progression of this disease. Discrete alterations in calcium signalling have been implicated in hormone-sensitive, castration-resistant and aggressive variant forms of prostate cancer. Hence, modulation of calcium signals and downstream effector molecules is a plausible therapeutic strategy for both early and late stages of prostate cancer. Based on this premise, clinical trials have been undertaken to establish the feasibility of targeting calcium signalling specifically for prostate cancer.

Indexed as

CalciumProstatic NeoplasmsHumansMaleOrchiectomySignal TransductionCalcium

Identifiers

PMID36964408
OpenAlexW4360826379

What Socratic 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 Socratic graph.