Evidence map›Paper›PMID 36497384›Full record

ReviewCancers2022

The Study of the Extracellular Matrix in Chronic Inflammation: A Way to Prevent Cancer Initiation?

Asia Marangio, Andrea Biccari, Edoardo D'Angelo, Francesca Sensi, Gaya Spolverato, Salvatore Pucciarelli, Marco Agostini

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Polynucleotide HPTAntioxidants (Basel, Switzerland) · 2025
    Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024
    Article
  12. Article
  13. 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

7 authors at 1 institution in 1 country.

Asia MarangioGeneral Surgery 3, Department of Surgery, Oncology and Gastroenterology, University of Padova, Via Giustiniani 2, 35128 Padova, Italy.
Andrea BiccariGeneral Surgery 3, Department of Surgery, Oncology and Gastroenterology, University of Padova, Via Giustiniani 2, 35128 Padova, Italy.
Edoardo D'AngeloGeneral Surgery 3, Department of Surgery, Oncology and Gastroenterology, University of Padova, Via Giustiniani 2, 35128 Padova, Italy.ORCID 0000-0002-4554-2140
Francesca SensiFondazione Istituto di Ricerca Pediatrica, Città della Speranza, 35129 Padova, Italy.
Gaya SpolveratoGeneral Surgery 3, Department of Surgery, Oncology and Gastroenterology, University of Padova, Via Giustiniani 2, 35128 Padova, Italy.
Salvatore PucciarelliGeneral Surgery 3, Department of Surgery, Oncology and Gastroenterology, University of Padova, Via Giustiniani 2, 35128 Padova, Italy.
Marco AgostiniGeneral Surgery 3, Department of Surgery, Oncology and Gastroenterology, University of Padova, Via Giustiniani 2, 35128 Padova, Italy.ORCID 0000-0001-7578-1233
University of Padua · IT

Funding

Progetto di Sviluppo Dipartimentale DISCOG (Progetto Biobanca Univesity of Padova) NA
6 · The paper itself

Abstract

Bidirectional communication between cells and their microenvironment has a key function in normal tissue homeostasis, and in disease initiation, progression and a patient's prognosis, at the very least. The extracellular matrix (ECM), as an element of all tissues and cellular microenvironment, is a frequently overlooked component implicated in the pathogenesis and progression of several diseases. In the inflammatory microenvironment (IME), different alterations resulting from remodeling processes can affect ECM, progressively inducing cancer initiation and the passage toward a tumor microenvironment (TME). Indeed, it has been demonstrated that altered ECM components interact with a variety of surface receptors triggering intracellular signaling that affect cellular pathways in turn. This review aims to support the notion that the ECM and its alterations actively participate in the promotion of chronic inflammation and cancer initiation. In conclusion, some data obtained in cancer research with the employment of decellularized ECM (dECM) models are described. The reported results encourage the application of dECM models to investigate the short circuits contributing to the creation of distinct IME, thus representing a potential tool to avoid the progression toward a malignant lesion.

Indexed as

3D culture modelcancerchronic inflammationdecellularizationextracellular matrix

Identifiers

PMID36497384
PMCPMC9741172
OpenAlexW4311009767

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.