Evidence map›Paper›PMID 28560038›Full record

ArticleMultidisciplinary respiratory medicine2017

Mutational status predicts the risk of thromboembolic events in lung adenocarcinoma.

Elsa Davidsson, Nicola Murgia, Cristian Ortiz-Villalón, Emil Wiklundh, Magnus Sköld, Karl Gustav Kölbeck, Giovanni Ferrara

Open access · goldAbstract read
In one paragraph

Article in Multidisciplinary respiratory medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 2 pooled it
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

16 citing papers in PubMed, 2 syntheses or guidelines pooled it, 29 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  7. Review
  8. Article
  9. Mechanisms of cancer-associated thrombosis.Research and practice in thrombosis and haemostasis · 2023
    Article
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  16. Cancer-associated thrombosis: The search for the holy grail continues.Research and practice in thrombosis and haemostasis · 2018
    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

7 authors at 2 institutions in 2 countries.

Elsa Davidsson *Department of Respiratory Medicine and Allergy, Karolinska University Hospital, Stockholm, Sweden.
Nicola Murgia *Section of Occupational Medicine, Respiratory Diseases and Toxicology, University of Perugia, Perugia, Italy.
Cristian Ortiz-VillalónDepartment of Pathology, Karolinska University Hospital, Stockholm, Sweden.
Emil WiklundhDepartment of Respiratory Medicine and Allergy, Karolinska University Hospital, Stockholm, Sweden.
Magnus SköldDepartment of Respiratory Medicine and Allergy, Karolinska University Hospital, Stockholm, Sweden.
Karl Gustav KölbeckDepartment of Respiratory Medicine and Allergy, Karolinska University Hospital, Stockholm, Sweden.
Giovanni FerraraDepartment of Respiratory Medicine and Allergy, Karolinska University Hospital, Stockholm, Sweden.ORCID 0000-0002-3807-3315
Karolinska University Hospital · SEUniversity of Perugia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPrecision medicine promises to improve prognosis of patients affected by untreatable diseases. Patients with lung cancer (especially lung adenocarcinoma) bear an increased risk of VTE. Mutations in the EGFR and rearrangement in the ALK genes identify specific subgroups of patients. Aim of this study was to investigate the role of epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK) mutational status on the risk of venous thromboembolism (VTE) in lung adenocarcinoma.

methodsA retrospective longitudinal design was used. Patients with lung adenocarcinoma diagnosed and undergoing a mutational analysis at the Karolinska University Hospital, Stockholm, Sweden between January 2009 and September 2015 were divided in three subgroups based on their mutational status (EGFR-, ALK-mutated, unexposed group). Event-free time for VTE was assessed using Cox regression analysis based on mutation status and treatment received.

resultsThree hundred-ten patients were included. A VTE occurred in 70 (22.6%) patients. Mutation of EGFR was associated with a decreased risk of VTE (HR 0.46, 95% CI 0.23-0.94). Treatment with tyrosine kinase inhibitors (TKI) reduced the risk of VTE compared to other treatment strategies not including TKI (HR 0.42, 95% CI 0.29-0.79).

conclusionsOur study suggests that patients with lung adenocarcinoma bearing a EGFR-mutation have a decreased risk of VTE compared with patients with other forms of lung adenocarcinoma. Targeted therapy with TKI alone or in combination with other treatments seems to reduce the risk of VTE compared to other treatments not including TKI.

Indexed as

MutationNon-small cell lung cancerPrecision medicineThromboembolismTyrosine kinase inhibitors

Identifiers

PMID28560038
PMCPMC5447302
OpenAlexW2616656876

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.