Evidence map›Paper›PMID 27590450›Full record

ReviewJournal of translational medicine2016

Ockham's razor for the MET-driven invasive growth linking idiopathic pulmonary fibrosis and cancer.

Giulia M Stella, Alessandra Gentile, Alice Balderacchi, Federica Meloni, Melissa Milan, Silvia Benvenuti

Erratum issuedOpen access · goldAbstract readReview
In one paragraph

Review in Journal of translational medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 16% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.

  1. Pooled it
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  3. Review
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  5. Article
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  7. Review
  8. Article
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  11. Therapeutic targeting of argininosuccinate synthase 1 (ASS1)-deficient pulmonary fibrosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2021
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

Giulia M StellaPneumology Unit, Cardiothoracic and Vascular Department, IRCCS Policlinico San Matteo Foundation and University of Pavia Medical School, Piazzale Golgi 19, 27100, Pavia, Italy. g.stella@smatteo.pv.it.
Alessandra GentileExperimental Clinical Molecular Oncology (ECMO), IRCCS Candiolo Cancer Institute-FPO, Candiolo, 20060, Turin, Italy.
Alice BalderacchiInvestigational Clinical Oncology (INCO), IRCCS Candiolo Cancer Institute-FPO, Candiolo, 20060, Turin, Italy.
Federica MeloniPneumology Unit, Cardiothoracic and Vascular Department, IRCCS Policlinico San Matteo Foundation and University of Pavia Medical School, Piazzale Golgi 19, 27100, Pavia, Italy.
Melissa MilanExperimental Clinical Molecular Oncology (ECMO), IRCCS Candiolo Cancer Institute-FPO, Candiolo, 20060, Turin, Italy.
Silvia BenvenutiExperimental Clinical Molecular Oncology (ECMO), IRCCS Candiolo Cancer Institute-FPO, Candiolo, 20060, Turin, Italy.
Candiolo Cancer Institute · ITIstituti di Ricovero e Cura a Carattere Scientifico · ITUniversity of Pavia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIdiopathic pulmonary fibrosis (IPF) identifies a specific lung disorder characterized by chronic, progressive fibrosing interstitial pneumonia of unknown etiology, which lacks effective treatment. According to the current pathogenic perspective, the aberrant proliferative events in IPF resemble those occurring during malignant transformation. MAIN BODY: Receptor tyrosine kinases (RTK) are known to be key players in cancer onset and progression. It has been demonstrated that RTK expression is sometimes also altered and even druggable in IPF. One example of an RTK-the MET proto-oncogene-is a key regulator of invasive growth. This physiological genetic program supports embryonic development and post-natal organ regeneration, as well as cooperating in the evolution of cancer metastasis when aberrantly activated. Growing evidence sustains that MET activation may collaborate in maintaining tissue plasticity and the regenerative potential that characterizes IPF.

conclusionThe present work aims to elucidate-by applying the logic of simplicity-the bio-molecular mechanisms involved in MET activation in IPF. This clarification is crucial to accurately design MET blockade strategies within a fully personalized approach to IPF.

Indexed as

Models, BiologicalAnimalsCell ProliferationHumansIdiopathic Pulmonary FibrosisLung NeoplasmsNeoplasm InvasivenessProto-Oncogene MasProto-Oncogene Proteins c-metMAS1 protein, humanProto-Oncogene MasProto-Oncogene Proteins c-metCancerEpithelial-to-mesenchymal transitionIdiopathic pulmonary fibrosisInvasive growthPrecision medicine

Identifiers

PMID27590450
PMCPMC5010719
OpenAlexW2508602072

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.