Evidence map›Paper›PMID 38852006›Full record

ArticleClinical lung cancer2024

Genomic and Immune Landscape Comparison of MET Exon 14 Skipping and MET-Amplified Non-small Cell Lung Cancer.

Rachel L Minne, Natalie Y Luo, Anne M Traynor, Minxuan Huang, Luisina DeTullio, Jen Godden, Melissa Stoppler, Randall J Kimple, Andrew M Baschnagel

Abstract readComparative Study
PubMed Full text at PMC Publisher
In one paragraph

Article in Clinical lung cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

  1. Article
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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

9 authors.

Rachel L MinneDepartment of Human Oncology, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin.
Natalie Y LuoDepartment of Human Oncology, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin.
Anne M TraynorUniversity of Wisconsin Carbone Cancer Center, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin; Department of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin.
Minxuan HuangTempus AI, Inc(.), Chicago, IL.
Luisina DeTullioTempus AI, Inc(.), Chicago, IL.
Jen GoddenTempus AI, Inc(.), Chicago, IL.
Melissa StopplerTempus AI, Inc(.), Chicago, IL.
Randall J KimpleDepartment of Human Oncology, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin; University of Wisconsin Carbone Cancer Center, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin.
Andrew M BaschnagelDepartment of Human Oncology, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin; University of Wisconsin Carbone Cancer Center, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin. Electronic address: baschnagel@humonc.wisc.edu.

Funding

UW COMPREHENSIVE CANCER CENTER SUPPORTP30CA014520 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI Justine Yang Bruce · 1985 to 2026
$142.6M
NCI NIH HHS P30 CA014520
6 · The paper itself

Abstract

backgroundMutation or amplification of the mesenchymal-epithelial transition (MET) tyrosine kinase receptor causes dysregulation of receptor function and stimulates tumor growth in non-small cell lung cancer (NSCLC) with the most common mutation being MET exon 14 (METex14). We sought to compare the genomic and immune landscape of MET-altered NSCLC with MET wild-type NSCLC.

methods18,047 NSCLC tumors were sequenced with Tempus xT assay. Tumors were categorized based on MET exon 14 (METex14) mutations; low MET amplification defined as a copy number gain (CNG) 6-9, high MET amplification defined as CNG ≥ 10, and MET other type mutations. Immuno-oncology (IO) biomarkers and the frequency of other somatic gene alterations were compared across MET-altered and MET wild-type groups.

results276 (1.53%) METex14, 138 (0.76%) high METamp, 63 (0.35%) low METamp, 27 (0.15%) MET other, and 17,543 (97%) MET wild-type were identified. Patients with any MET mutation including METex14 were older, while patients with METex14 were more frequently female and nonsmokers. MET gene expression was highest in METamp tumors. PD-L1 positivity rates were higher in MET-altered groups than MET wild-type. METex14 exhibited the lowest tumor mutational burden (TMB) and lowest neoantigen tumor burden (NTB). METamp exhibited the lowest proportion of CD4 T cells and the highest proportion of NK cells. There were significant differences in co-alterations between METamp and METex14.

conclusionsMETex14 tumors exhibited differences in IO biomarkers and the somatic landscape compared to non-METex14 NSCLC tumors. Variations in immune profiles can affect immunotherapy selection in MET-altered NSCLC and require further exploration.

Indexed as

Carcinoma, Non-Small-Cell LungExonsLung NeoplasmsMutationProto-Oncogene Proteins c-metAgedBiomarkers, TumorFemaleGene AmplificationGenomicsHumansMaleMiddle AgedBiomarkers, TumorMET protein, humanProto-Oncogene Proteins c-metCancer genomicsImmune biomarkersMET amplification

Identifiers

PMID38852006
PMCPMC12121485

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