Evidence map›Paper›PMID 33110136›Full record

ArticleScientific reports2020

Modulation of complement activation by pentraxin-3 in prostate cancer.

Giovanni Stallone, Giuseppe Stefano Netti, Luigi Cormio, Giuseppe Castellano, Barbara Infante, Paola Pontrelli, Chiara Divella, Oscar Selvaggio, Federica Spadaccino, Elena Ranieri and 5 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. 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
1.3field-weighted citation impact, top 19% 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, 30 citations in OpenAlex.

  1. Review
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  10. Article
  11. Article
  12. Article
  13. Role of long pentraxin PTX3 in cancer.Clinical and experimental medicine · 2023
    Review
  14. Article
  15. Review
  16. Review
  17. Insights into the Relationship between Pentraxin-3 and Cancer.International journal of molecular sciences · 2022
    Review
  18. Review
  19. Article
  20. Inside-Out of Complement in Cancer.Frontiers in immunology · 2022
    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

15 authors at 3 institutions in 1 country.

Giovanni StalloneNephrology Dialysis and Transplantation Unit, University of Foggia, Viale Luigi Pinto, 251, 71122, Foggia, Italy. giovanni.stallone@unifg.it.
Giuseppe Stefano NettiClinical Pathology Unit, Department of Medical and Surgical Sciences, University of Foggia, Viale Luigi Pinto, 251, 71122, Foggia, Italy.
Luigi CormioUrology and Renal Transplantation Unit, University of Foggia, Viale Luigi Pinto, 251, 71122, Foggia, Italy.
Giuseppe CastellanoNephrology Dialysis and Transplantation Unit, University of Foggia, Viale Luigi Pinto, 251, 71122, Foggia, Italy.
Barbara InfanteNephrology Dialysis and Transplantation Unit, University of Foggia, Viale Luigi Pinto, 251, 71122, Foggia, Italy.
Paola PontrelliNephrology, Dialysis and Transplantation Unit, Department of Emergency and Organ Transplantation, University of Bari "Aldo Moro", Bari, Italy.
Chiara DivellaNephrology, Dialysis and Transplantation Unit, Department of Emergency and Organ Transplantation, University of Bari "Aldo Moro", Bari, Italy.
Oscar SelvaggioUrology and Renal Transplantation Unit, University of Foggia, Viale Luigi Pinto, 251, 71122, Foggia, Italy.
Federica SpadaccinoClinical Pathology Unit, Department of Medical and Surgical Sciences, University of Foggia, Viale Luigi Pinto, 251, 71122, Foggia, Italy.
Elena RanieriClinical Pathology Unit, Department of Medical and Surgical Sciences, University of Foggia, Viale Luigi Pinto, 251, 71122, Foggia, Italy.
Francesca SanguedolcePathology Unit, Department of Clinical and Experimental Medicine, University of Foggia, Viale Luigi Pinto, 251, 71122, Foggia, Italy.
Antonio PennellaPathology Unit, Department of Clinical and Experimental Medicine, University of Foggia, Viale Luigi Pinto, 251, 71122, Foggia, Italy.
Loreto GesualdoNephrology, Dialysis and Transplantation Unit, Department of Emergency and Organ Transplantation, University of Bari "Aldo Moro", Bari, Italy.
Giuseppe CarrieriUrology and Renal Transplantation Unit, University of Foggia, Viale Luigi Pinto, 251, 71122, Foggia, Italy.
Giuseppe GrandalianoFondazione Policlinico Universitario A. Gemelli IRCCS, Largo A. Gemelli 8, 00168, Rome, Italy.
University of Foggia · ITUniversity of Bari Aldo Moro · ITAgostino Gemelli University Polyclinic · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pentraxin 3 (PTX3) is an essential component of the innate immune system and a recognized modulator of Complement cascade. The role of Complement system in the pathogenesis of prostate cancer has been largely underestimated. The aim of our study was to investigate the role of PTX3 as possible modulator of Complement activation in the development of this neoplasia. We performed a single center cohort study; from January 2017 through December 2018, serum and prostate tissue samples were obtained from 620 patients undergoing prostate biopsy. A group of patients with benign prostatic hyperplasia (BPH) underwent a second biopsy within 12-36 months demonstrating the presence of a prostate cancer (Group A, n = 40) or confirming the diagnosis of BPH (Group B, N = 40). We measured tissue PTX3 protein expression together with complement activation by confocal microscopy in the first and second biopsy in group A and B patients. We confirmed that that PTX3 tissue expression in the first biopsy was increased in group A compared to group B patients. C1q deposits were extensively present in group A patients co-localizing and significantly correlating with PTX3 deposits; on the contrary, C1q/PTX3 deposits were negative in group B. Moreover, we found a significantly increased expression of C3a and C5a receptors within resident cells in group A patient. Interestingly, C1q/PTX3 deposits were not associated with activation of the terminal Complement complex C5b-9; moreover, we found a significant increase of Complement inhibitor CD59 in cancer tissue. Our data indicate that PTX3 might play a significant pathogenic role in the development of this neoplasia through recruitment of the early components of Complement cascade with hampered activation of terminal Complement pathway associated with the upregulation of CD59. This alteration might lead to the PTX3-mediated promotion of cellular proliferation, angiogenesis and insensitivity to apoptosis possible leading to cancer cell invasion and migration.

Indexed as

Acute-Phase ProteinsCohort StudiesComplement ActivationC-Reactive ProteinHumansMalePentraxinsProstatic NeoplasmsSerum Amyloid P-ComponentAcute-Phase ProteinsC-Reactive ProteinPentraxinsSerum Amyloid P-Component

Identifiers

PMID33110136
PMCPMC7591881
OpenAlexW3095876941

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.