Evidence map›Paper›PMID 31199580›Full record

ArticleCancer medicine2019

NF1 mutations identify molecular and clinical subtypes of lung adenocarcinomas.

Camille Tlemsani, Nicolas Pécuchet, Aurelia Gruber, Ingrid Laurendeau, Claire Danel, Marc Riquet, Françoise Le Pimpec-Barthes, Elizabeth Fabre, Audrey Mansuet-Lupo, Diane Damotte and 13 more

Open access · goldAbstract read
In one paragraph

Article in Cancer medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.2field-weighted citation impact, top 19% 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, 18 citations in OpenAlex.

  1. The Current Roadmap of Lung Cancer Biology, Genomics and Racial Disparity.International journal of molecular sciences · 2025
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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

23 authors at 5 institutions in 1 country.

Camille TlemsaniService de Génétique et Biologie Moléculaires, Hôpital Cochin, Hôpitaux Universitaires Paris Centre, Assistance Publique-Hôpitaux de Paris (AP-HP), Paris, France.ORCID 0000-0002-3342-1704
Nicolas PécuchetINSERM UMR-S1147, Université Sorbonne-Paris-Cité, Paris, France.
Aurelia GruberEA7331, Faculté de Pharmacie de Paris, Université Paris Descartes, Paris, France.
Ingrid LaurendeauEA7331, Faculté de Pharmacie de Paris, Université Paris Descartes, Paris, France.
Claire DanelService d'Anatomopathologie, Hôpital Bichat, AP-HP, Paris, France.
Marc RiquetService de Chirurgie Thoracique, Hôpital Européen Georges Pompidou (HEGP), AP-HP, Paris, France.
Françoise Le Pimpec-BarthesService de Chirurgie Thoracique, Hôpital Européen Georges Pompidou (HEGP), AP-HP, Paris, France.
Elizabeth FabreINSERM UMR-S1147, Université Sorbonne-Paris-Cité, Paris, France.
Audrey Mansuet-LupoService d'Anatomopathologie, Hôpital Cochin, Hôpitaux Universitaires Paris Centre, AP-HP, Paris, France.
Diane DamotteService d'Anatomopathologie, Hôpital Cochin, Hôpitaux Universitaires Paris Centre, AP-HP, Paris, France.
Marco AlifanoService de Chirurgie Thoracique, Hôpital Cochin, Hôpitaux Universitaires Paris Centre, AP-HP, Paris, France.ORCID 0000-0002-2038-1037
Armelle LuscanService de Génétique et Biologie Moléculaires, Hôpital Cochin, Hôpitaux Universitaires Paris Centre, Assistance Publique-Hôpitaux de Paris (AP-HP), Paris, France.
Benoit RousseauService d'Oncologie Médicale, hôpital Henri-Mondor, AP-HP, Créteil, France.
Dominique VidaudService de Génétique et Biologie Moléculaires, Hôpital Cochin, Hôpitaux Universitaires Paris Centre, Assistance Publique-Hôpitaux de Paris (AP-HP), Paris, France.
Jennifer VarinEA7331, Faculté de Pharmacie de Paris, Université Paris Descartes, Paris, France.
Beatrice ParfaitService de Génétique et Biologie Moléculaires, Hôpital Cochin, Hôpitaux Universitaires Paris Centre, Assistance Publique-Hôpitaux de Paris (AP-HP), Paris, France.
Ivan BiecheEA7331, Faculté de Pharmacie de Paris, Université Paris Descartes, Paris, France.
Karen LeroyService de Génétique et Biologie Moléculaires, Hôpital Cochin, Hôpitaux Universitaires Paris Centre, Assistance Publique-Hôpitaux de Paris (AP-HP), Paris, France.
Pierre Laurent-PuigINSERM UMR-S1147, Université Sorbonne-Paris-Cité, Paris, France.
Benoit TerrisService d'Anatomopathologie, Hôpital Cochin, Hôpitaux Universitaires Paris Centre, AP-HP, Paris, France.
Helene BlonsINSERM UMR-S1147, Université Sorbonne-Paris-Cité, Paris, France.
Michel VidaudService de Génétique et Biologie Moléculaires, Hôpital Cochin, Hôpitaux Universitaires Paris Centre, Assistance Publique-Hôpitaux de Paris (AP-HP), Paris, France.
Eric PasmantService de Génétique et Biologie Moléculaires, Hôpital Cochin, Hôpitaux Universitaires Paris Centre, Assistance Publique-Hôpitaux de Paris (AP-HP), Paris, France.
Délégation Paris 5 · FRHôpital Cochin · FRInserm · FRHôpital Européen Georges-Pompidou · FRHôpital Bichat-Claude-Bernard · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The tumor suppressor gene neurofibromin 1 (NF1) is a major regulator of the RAS-MAPK pathway. NF1 mutations occur in lung cancer but were not extensively explored. We hypothesized that NF1-mutated tumors could define a specific population with a distinct clinical and molecular profile. We performed NF1 sequencing using next generation sequencing (NGS) in 154 lung adenocarcinoma surgical specimens with known KRAS, EGFR, TP53, BRAF, HER2, and PIK3CA status, to evaluate the molecular and clinical specificities of NF1-mutated lung cancers. Clinical data were retrospectively collected, and their associations with molecular profiles assessed. In this series, 24 tumors were NF1 mutated (17.5%) and 11 were NF1 deleted (8%). There was no mutation hotspot. NF1 mutations were rarely associated with other RAS-MAPK pathway mutations. Most of patients with NF1 alterations were males (74.3%) and smokers (74.3%). Overall survival and disease-free survival were statistically better in patients with NF1 alterations (N = 34) than in patients with KRAS mutations (N = 30) in univariate analysis. Our results confirm that NF1 is frequently mutated and represents a distinct molecular and clinical subtype of lung adenocarcinoma.

Indexed as

MutationAdenocarcinoma of LungAdultAgedAged, 80 and overFemaleHigh-Throughput Nucleotide SequencingHumansLung NeoplasmsMaleMAP Kinase Signaling SystemMiddle AgedNeoplasm StagingNeurofibromin 1PrognosisRetrospective StudiesNeurofibromin 1NF1 protein, humanlung adenocarcinomamolecular subtypenext generation sequencingNF1RAS-MAPK pathway

Identifiers

PMID31199580
PMCPMC6675708
OpenAlexW2950407919

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.