Evidence map›Paper›PMID 32791233›Full record

ArticleJournal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer2020

The Underlying Tumor Genomics of Predominant Histologic Subtypes in Lung Adenocarcinoma.

Raul Caso, Francisco Sanchez-Vega, Kay See Tan, Brooke Mastrogiacomo, Jian Zhou, Gregory D Jones, Bastien Nguyen, Nikolaus Schultz, James G Connolly, Whitney S Brandt and 9 more

Open access · greenAbstract read
In one paragraph

Article in Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers.

0numbers the graph read from it
0cells of the map it votes in
97citing papers in PubMed
8.3field-weighted citation impact, top 1% 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

97 citing papers in PubMed, 166 citations in OpenAlex.

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37 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

19 authors at 2 institutions in 1 country.

Raul CasoThoracic Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, New York.
Francisco Sanchez-VegaColorectal Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, New York; Computational Oncology Service, Department of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, New York.
Kay See TanDepartment of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, New York.
Brooke MastrogiacomoThoracic Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, New York; Computational Oncology Service, Department of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, New York.
Jian ZhouThoracic Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, New York.
Gregory D JonesThoracic Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, New York.
Bastien NguyenMarie-Josée and Henry R. Kravis Center for Molecular Oncology, Memorial Sloan Kettering Cancer Center, New York, New York.
Nikolaus SchultzMarie-Josée and Henry R. Kravis Center for Molecular Oncology, Memorial Sloan Kettering Cancer Center, New York, New York.
James G ConnollyThoracic Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, New York.
Whitney S BrandtThoracic Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, New York.
Matthew J BottThoracic Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, New York; Fiona and Stanley Druckenmiller Center for Lung Cancer Research, Memorial Sloan Kettering Cancer Center, New York, New York.
Gaetano RoccoThoracic Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, New York; Fiona and Stanley Druckenmiller Center for Lung Cancer Research, Memorial Sloan Kettering Cancer Center, New York, New York.
Daniela MolenaThoracic Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, New York; Fiona and Stanley Druckenmiller Center for Lung Cancer Research, Memorial Sloan Kettering Cancer Center, New York, New York.
James M IsbellThoracic Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, New York; Fiona and Stanley Druckenmiller Center for Lung Cancer Research, Memorial Sloan Kettering Cancer Center, New York, New York.
Yuan LiuThoracic Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, New York; Fiona and Stanley Druckenmiller Center for Lung Cancer Research, Memorial Sloan Kettering Cancer Center, New York, New York.
Marty W MayoDepartment of Biochemistry & Molecular Genetics, University of Virginia, Virginia.
Prasad S AdusumilliThoracic Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, New York; Fiona and Stanley Druckenmiller Center for Lung Cancer Research, Memorial Sloan Kettering Cancer Center, New York, New York.
William D TravisFiona and Stanley Druckenmiller Center for Lung Cancer Research, Memorial Sloan Kettering Cancer Center, New York, New York; Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, New York.
David R JonesThoracic Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, New York; Fiona and Stanley Druckenmiller Center for Lung Cancer Research, Memorial Sloan Kettering Cancer Center, New York, New York. Electronic address: jonesd2@mskcc.org.
Memorial Sloan Kettering Cancer Center · USUniversity of Virginia · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
SURGICAL ONCOLOGY RESEARCH TRAINING PROGRAMT32CA009501 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Babak J Mehrara · 1985 to 2026
$7.7M
BRMS1-mediated suppression of metastases in p53 mutant lung adenocarcinomaR01CA217169 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI JONES, DAVID R · 2018 to 2022
$2.5M
Targeting SNP BRMS1v2 A273V/A273V to reduce metastases in lung adenocarcinomaR01CA240472 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI JONES, DAVID R · 2019 to 2023
$2.4M
Image-guided irreversible electroporation directed CAR T-cell delivery to solid tumorsR01CA236615 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI ADUSUMILLI, PRASAD S., SOLOMON, STEPHEN BARNETT · 2018 to 2022
$2.0M
Identifying tumor suppressor targets of SIRT6 in lung cancerR01CA192399 · NCI · UNIVERSITY OF VIRGINIA · PI MAYO, MARTY W · 2015 to 2019
$1.9M
NCATS NIH HHS UL1 TR001863NCI NIH HHS P30 CA008748NCI NIH HHS R01 CA192399NCI NIH HHS R01 CA217169NCI NIH HHS R01 CA236615NCI NIH HHS R01 CA240472NCI NIH HHS T32 CA009501
6 · The paper itself

Abstract

introductionThe purpose of the study is to genomically characterize the biology and related therapeutic opportunities of prognostically important predominant histologic subtypes in lung adenocarcinoma (LUAD).

methodsWe identified 604 patients with stage I to III LUAD who underwent complete resection and targeted next-generation sequencing using the Memorial Sloan Kettering-Integrated Mutation Profiling of Actionable Cancer Targets platform. Tumors were classified according to predominant histologic subtype and grouped by architectural grade (lepidic [LEP], acinar or papillary [ACI/PAP], and micropapillary or solid [MIP/SOL]). Associations among clinicopathologic factors, genomic features, mutational signatures, and recurrence were evaluated within subtypes and, when appropriate, quantified using competing-risks regression, with adjustment for pathologic stage and extent of resection.

resultsMIP/SOL tumors had higher tumor mutational burden (p < 0.001), fraction of genome altered (p = 0.001), copy number amplifications (p = 0.021), rate of whole-genome doubling (p = 0.008), and number of oncogenic pathways altered ( p < 0.001) as compared with LEP and ACI/PAP tumors. Across all tumors, mutational signatures attributed to APOBEC activity were associated with the highest risk of postresection recurrence: SBS2 (p = 0.021) and SBS13 (p = 0.005). Three oncogenic pathways (p53, Wnt, Myc) were altered with statistical significance in MIP/SOL tumors. Compared with LEP and ACI/PAP tumors, MIP/SOL tumors had a higher frequency of targetable BRAF-V600E mutations (p = 0.046). Among ACI/PAP tumors, alterations in the cell cycle (p < 0.001) and PI3K (p = 0.002) pathways were associated with recurrence; among MIP/SOL tumors, only PI3K alterations were associated with recurrence (p = 0.049).

conclusionsThese results provide the first in-depth assessment of tumor genomic profiling of predominant LUAD histologic subtypes, their associations with recurrence, and their correlation with targetable driver alterations in patients with surgically resected LUAD.

Indexed as

Lung NeoplasmsAdenocarcinoma of LungAgedFemaleGenomicsHumansMaleMiddle AgedMutationNeoplasm Recurrence, LocalPrognosisHistologic subtypesLung adenocarcinomaNext-generation sequencingTumor genomic profiling

Identifiers

PMID32791233
PMCPMC7704768
OpenAlexW3048243382

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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.