Evidence map›Paper›PMID 35598205›Full record

ArticleThe oncologist2022

Clinicopathologic and Genomic Landscape of Non-Small Cell Lung Cancer Brain Metastases.

Richard S P Huang, Lukas Harries, Brennan Decker, Matthew C Hiemenz, Karthikeyan Murugesan, James Creeden, Khaled Tolba, Laura P Stabile, Shakti H Ramkissoon, Timothy F Burns and 1 more

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PubMed Full text at PMC Publisher
In one paragraph

Article in The oncologist, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
–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

33 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Non-small cell lung cancer withFrontiers in oncology · 2023
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  13. Identifying the genomic landscape of EGFR-mutant lung cancers with central nervous system metastases.Annals of oncology : official journal of the European Society for Medical Oncology · 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

11 authors.

Richard S P HuangFoundation Medicine, Inc., Cambridge, MA, USA.ORCID 0000-0001-8395-5168
Lukas HarriesFoundation Medicine, Inc., Cambridge, MA, USA.
Brennan DeckerFoundation Medicine, Inc., Cambridge, MA, USA.
Matthew C HiemenzFoundation Medicine, Inc., Cambridge, MA, USA.
Karthikeyan MurugesanFoundation Medicine, Inc., Cambridge, MA, USA.
James CreedenFoundation Medicine, Inc., Cambridge, MA, USA.
Khaled TolbaFoundation Medicine, Inc., Cambridge, MA, USA.
Laura P StabileUniversity of Pittsburgh Medical Center (UPMC) Hillman Cancer Center, University of Pittsburgh, Pittsburgh, PA, USA.
Shakti H RamkissoonFoundation Medicine, Inc., Cambridge, MA, USA.
Timothy F BurnsUniversity of Pittsburgh Medical Center (UPMC) Hillman Cancer Center, University of Pittsburgh, Pittsburgh, PA, USA.
Jeffrey S RossFoundation Medicine, Inc., Cambridge, MA, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIn patients with non-small cell lung cancer (NSCLC), 10%-40% will eventually develop brain metastases. We present the clinicopathologic, genomic, and biomarker landscape of a large cohort of NSCLC brain metastases (NSCLC-BM) samples. MATERIALS AND

methodsWe retrospectively analyzed 3035 NSCLC-BM tested with comprehensive genomic profiling (CGP) during routine clinical care. In addition, we compared the NSCLC-BM to a separate cohort of 7277 primary NSCLC (pNSCLC) specimens. Finally, we present data on 67 paired patients with NSCLC-BM and pNSCLC.

resultsComprehensive genomic profiling analysis of the 3035 NSCLC-BMs found that the most frequent genomic alterations (GAs) were in the TP53, KRAS, CDKN2A, STK11, CDKN2B, EGFR, NKX2-1, RB1, MYC, and KEAP1 genes. In the NSCLC-BM cohort, there were significantly higher rates of several targetable GAs compared with pNSCLC, including ALK fusions, KRAS G12C mutations, and MET amplifications; and decreased frequency of MET exon14 skipping mutations (all P < .05). In the subset of NSCLC-BM (n = 1063) where concurrent PD-L1 immunohistochemistry (IHC) was performed, 54.7% of the patients with NSCLC-BM were eligible for pembrolizumab based on PD-L1 IHC (TPS ≥ 1), and 56.9% were eligible for pembrolizumab based on TMB-High status. In addition, in a series 67 paired pNSCLC and NSCLC-BM samples, 85.1% (57/67) had at least one additional GA discovered in the NSCLC-BM sample when compared with the pNSCLC sample.

conclusionsHerein, we defined the clinicopathologic, genomic, and biomarker landscape of a large cohort of patients with NSCLC-BM which can help inform study design of future clinical studies for patients with NSCLC with BM. In certain clinical situations, metastatic NSCLC brain tissue or cerebral spinal fluid specimens may be needed to fully optimize personalized treatment.

Indexed as

Brain NeoplasmsCarcinoma, Non-Small-Cell LungLung NeoplasmsB7-H1 AntigenErbB ReceptorsGenomicsHumansKelch-Like ECH-Associated Protein 1MutationNF-E2-Related Factor 2Proto-Oncogene Proteins p21(ras)Receptor Protein-Tyrosine KinasesRetrospective StudiesB7-H1 AntigenErbB ReceptorsKelch-Like ECH-Associated Protein 1NF-E2-Related Factor 2Proto-Oncogene Proteins p21(ras)Receptor Protein-Tyrosine Kinasesbrain metastasisgenomicnon-small cell lung cancer

Identifiers

PMID35598205
PMCPMC9526503

What OpenQuestion holds

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Registered trials

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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.