Evidence map›Paper›PMID 27545006›Full record

ArticleScientific reports2016

Elucidating Genomic Characteristics of Lung Cancer Progression from In Situ to Invasive Adenocarcinoma.

Chanida Vinayanuwattikun, Florence Le Calvez-Kelm, Behnoush Abedi-Ardekani, David Zaridze, Anush Mukeria, Catherine Voegele, Maxime Vallée, Dewajani Purnomosari, Nathalie Forey, Geoffroy Durand and 4 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

37 citing papers in PubMed, 52 citations in OpenAlex.

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  8. Investigation ofHeliyon · 2024
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  17. Molecular Pathology of Lung Cancer.Cold Spring Harbor perspectives in medicine · 2022
    Review
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  19. Article
  20. 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

14 authors at 5 institutions in 5 countries.

Chanida VinayanuwattikunInternational Agency for Research on Cancer, Lyon, France.
Florence Le Calvez-KelmInternational Agency for Research on Cancer, Lyon, France.
Behnoush Abedi-ArdekaniInternational Agency for Research on Cancer, Lyon, France.
David ZaridzeRussian N.N. Blokhin Cancer Research Centre, Moscow, Russian Federation.
Anush MukeriaRussian N.N. Blokhin Cancer Research Centre, Moscow, Russian Federation.
Catherine VoegeleInternational Agency for Research on Cancer, Lyon, France.
Maxime ValléeInternational Agency for Research on Cancer, Lyon, France.
Dewajani PurnomosariInternational Agency for Research on Cancer, Lyon, France.
Nathalie ForeyInternational Agency for Research on Cancer, Lyon, France.
Geoffroy DurandInternational Agency for Research on Cancer, Lyon, France.
Graham ByrnesInternational Agency for Research on Cancer, Lyon, France.
James MckayInternational Agency for Research on Cancer, Lyon, France.
Paul BrennanInternational Agency for Research on Cancer, Lyon, France.
Ghislaine SceloInternational Agency for Research on Cancer, Lyon, France.
Centre International de Recherche sur le Cancer · FRRussian Cancer Research Center NN Blokhin · RUKing Chulalongkorn Memorial Hospital · THUniversitas Gadjah Mada · IDUniversité Laval · CA

Funding

World Health Organization 001
6 · The paper itself

Abstract

To examine the diversity of somatic alterations and clonal evolution according to aggressiveness of disease, nineteen tumor-blood pairs of 'formerly bronchiolo-alveolar carcinoma (BAC)' which had been reclassified into preinvasive lesion (adenocarcinoma in situ; AIS), focal invasive lesion (minimally invasive adenocarcinoma; MIA), and invasive lesion (lepidic predominant adenocarcinoma; LPA and non-lepidic predominant adenocarcinoma; non-LPA) according to IASLC/ATS/ERS 2011 classification were explored by whole exome sequencing. Several distinct somatic alterations were observed compare to the lung adenocarcinoma study from the Cancer Genome Atlas (TCGA). There were higher numbers of tumors with significant APOBEC mutation fold enrichment (73% vs. 58% TCGA). The frequency of KRAS mutations was lower in our study (5% vs. 32% TCGA), while a higher number of mutations of RNA-splicing genes, RBM10 and U2AF1, were found (37% vs. 11% TCGA). We found neither mutational pattern nor somatic copy number alterations that were specific to AIS/MIA. We demonstrated that clonal cell fraction was the only distinctive feature that discriminated LPA/non-LPA from AIS/MIA. The broad range of clonal frequency signified a more branched clonal evolution at the time of diagnosis. Assessment of tumor clonal cell fraction might provide critical information for individualized therapy as a prognostic factor, however this needs further study.

Indexed as

MutationAdenocarcinomaAgedAPOBEC DeaminasesFemaleHumansLung NeoplasmsMaleMiddle AgedNeoplasm InvasivenessProto-Oncogene Proteins p21(ras)APOBEC DeaminasesKRAS protein, humanProto-Oncogene Proteins p21(ras)

Identifiers

PMID27545006
PMCPMC4992872
OpenAlexW2507857874

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.