Evidence map›Paper›PMID 32599981›Full record

ArticleCancer research and treatment2020

Genetic Alterations in Preinvasive Lung Synchronous Lesions.

Soyeon Ahn, Jisun Lim, Soo Young Park, Hyojin Kim, Hyun Jung Kwon, Yeon Bi Han, Choon-Taek Lee, Sukki Cho, Jin-Haeng Chung

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer research and treatment, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.2field-weighted citation impact, top 53% 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

4 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. 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

9 authors at 1 institution in 1 country.

Soyeon AhnDivision of Statistics, Medical Research Collaborating Center, Seoul National University Bundang Hospital, Seongnam, Korea.
Jisun LimDivision of Statistics, Medical Research Collaborating Center, Seoul National University Bundang Hospital, Seongnam, Korea.
Soo Young ParkDepartment of Pathology and Translational Medicine, Seoul National University Bundang Hospital, Seongnam, Korea.
Hyojin KimDepartment of Pathology and Translational Medicine, Seoul National University Bundang Hospital, Seongnam, Korea.
Hyun Jung KwonDepartment of Pathology and Translational Medicine, Seoul National University Bundang Hospital, Seongnam, Korea.
Yeon Bi HanDepartment of Pathology and Translational Medicine, Seoul National University Bundang Hospital, Seongnam, Korea.
Choon-Taek LeeDepartment of Internal Medicine, Seoul National University Bundang Hospital, Seongnam, Korea.
Sukki ChoDepartment of Thoracic and Cardiovascular Surgery, Seoul National University Bundang Hospital, Seongnam, Korea.
Jin-Haeng ChungDepartment of Pathology and Translational Medicine, Seoul National University Bundang Hospital, Seongnam, Korea.
Seoul National University Bundang Hospital · KR

Funding

National Research Foundation of Korea NRF-2015R1D1A1A02061597Seoul National University Bundang Hospital 13-2016-013 to JHC
6 · The paper itself

Abstract

purposeDespite advances in treatment, lung cancer remains the leading cause of cancer mortality. This study aimed to characterise genome-wide tumorigenesis events and to understand the hypothesis of the multistep carcinogenesis of lung adenocarcinoma (LUAD). MATERIALS AND

methodsWe conducted multiregion whole-exome sequencing of LUAD with synchronous atypical adenomatous hyperplasia (AAH), adenocarcinoma in situ, or minimally invasive adenocarcinoma of 19 samples from three patients to characterize genome-wide tumorigenesis events and validate the hypothesis of the multistep carcinogenesis of LUAD. We identified potential pathogenic mutations preserved in preinvasive lesions and supplemented the finding by allelic variant level from RNA sequencing.

resultsOverall, independent mutational profiles were observed per patient and between patients. Some shared mutations including epidermal growth factor receptor (EGFR , p.L858R) were present across synchronous lesions.

conclusionHere, we show that there are driver gene mutations in AAH, and they may exacerbate as a sequence in a histological continuum, supporting the Darwinian evolution model of cancer genome. The intertumoral and intratumoral heterogeneity of synchronous LUAD implies that multi-biomarker strategies might be necessary for appropriate treatment.

Indexed as

Adenocarcinoma in SituAdenocarcinoma of LungAgedAged, 80 and overBiomarkers, TumorCarcinogenesisExome SequencingFemaleGenetic HeterogeneityHumansLungLung NeoplasmsMaleMiddle AgedMutationNeoplasms, Multiple PrimaryBiomarkers, TumorAdenocarcinoma of lungAtypical adenomatous hyperplasiaClonal evolutionMutationWhole exome sequencing

Identifiers

PMID32599981
PMCPMC7577825
OpenAlexW3033905785

What OpenQuestion holds

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LicenceCC BY-NC
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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.