Evidence map›Paper›PMID 40563468›Full record

ReviewBiomolecules2025

Mechanisms of Lung Cancer Development in Cystic Fibrosis Patients: The Role of Inflammation, Oxidative Stress, and Lung Microbiome Dysbiosis.

Raffaella Pagliaro, Filippo Scialò, Angela Schiattarella, Roberta Cianci, Susan F M Campbell, Fabio Perrotta, Andrea Bianco, Giuseppe Castaldo

Abstract readReview
In one paragraph

Review in Biomolecules, 2025. 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
–field-weighted citation impact
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.

  1. Article
  2. High-Penetrance Rare Variants Underlying Familial Lung Cancer Risk: Insights From Genetic Epidemiology of Lung Cancer Consortium.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2026
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  4. Review
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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

8 authors.

Raffaella PagliaroDepartment of Translational Medical Sciences, University of Campania 'L. Vanvitelli', 80131 Naples, Italy.ORCID 0009-0006-2902-3558
Filippo ScialòDepartment of Molecular Medicine and Medical Biotechnologies, University of Naples Federico II, 80131 Naples, Italy.ORCID 0000-0002-1121-7315
Angela SchiattarellaDepartment of Translational Medical Sciences, University of Campania 'L. Vanvitelli', 80131 Naples, Italy.
Roberta CianciU.O.C. Clinica Pneumologica L. Vanvitelli, A.O. dei Colli, Monaldi Hospital, 80131 Naples, Italy.
Susan F M CampbellDepartment of Translational Medical Sciences, University of Campania 'L. Vanvitelli', 80131 Naples, Italy.ORCID 0009-0005-3667-9902
Fabio PerrottaDepartment of Translational Medical Sciences, University of Campania 'L. Vanvitelli', 80131 Naples, Italy.
Andrea BiancoDepartment of Translational Medical Sciences, University of Campania 'L. Vanvitelli', 80131 Naples, Italy.ORCID 0000-0002-4692-5901
Giuseppe CastaldoDepartment of Molecular Medicine and Medical Biotechnologies, University of Naples Federico II, 80131 Naples, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cystic fibrosis (CF) is a genetic disorder caused by mutations in the CFTR gene, leading to defective ion transport and impaired function of various organs. Chronic inflammation, oxidative stress, and microbial dysbiosis are key pathological features of CF patients, contributing to disease progression, lung damage, and an increased susceptibility to infections. Emerging evidence suggests that in CF patients these factors can promote cancer development, especially lung cancer. Chronic inflammation in CF, driven by immune cell dysfunction, results in the release of pro-inflammatory cytokines and reactive oxygen species (ROSs), fostering an environment conducive to cancer initiation. Oxidative stress can amplify cellular damage and hinder airway remodeling. ROSs not only damage cellular components such as lipids, proteins, and DNA but also disrupt lung homeostasis, creating a favorable environment for cancer development. Furthermore, the lung microbiome in CF patients is often dysbiotic, with a reduced diversity and the predominance of pathogenic bacteria such as

Indexed as

Cystic FibrosisDysbiosisInflammationLungLung NeoplasmsMicrobiotaOxidative StressAnimalsHumanschronic inflammationcystic fibrosislung cancermicrobiome dysbiosisoxidative stress

Identifiers

PMID40563468
PMCPMC12190827

What OpenQuestion holds

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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.