Evidence map›Paper›PMID 37452277›Full record

ArticleBMC cancer2023

Common driver mutations and programmed death-ligand 1 expression in advanced non-small cell lung cancer in smokers and never smokers.

Chong Kin Liam, Chian Yih Yew, Yong Kek Pang, Chee Kuan Wong, Mau Ern Poh, Jiunn Liang Tan, Chun Ian Soo, Thian Chee Loh, Ka Kiat Chin, Vijayan Munusamy and 2 more

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

9 citing papers in PubMed, 11 citations in OpenAlex.

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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

12 authors at 2 institutions in 1 country.

Chong Kin LiamDepartment of Medicine, Faculty of Medicine, University of Malaya, 50603, Kuala Lumpur, Malaysia. liamck@ummc.edu.my.
Chian Yih YewDepartment of Medicine, University of Malaya Medical Centre, 59100, Kuala Lumpur, Malaysia.
Yong Kek PangDepartment of Medicine, Faculty of Medicine, University of Malaya, 50603, Kuala Lumpur, Malaysia.
Chee Kuan WongDepartment of Medicine, Faculty of Medicine, University of Malaya, 50603, Kuala Lumpur, Malaysia.
Mau Ern PohDepartment of Medicine, Faculty of Medicine, University of Malaya, 50603, Kuala Lumpur, Malaysia.
Jiunn Liang TanDepartment of Medicine, University of Malaya Medical Centre, 59100, Kuala Lumpur, Malaysia.
Chun Ian SooDepartment of Medicine, Faculty of Medicine, University of Malaya, 50603, Kuala Lumpur, Malaysia.
Thian Chee LohDepartment of Medicine, Faculty of Medicine, University of Malaya, 50603, Kuala Lumpur, Malaysia.
Ka Kiat ChinDepartment of Medicine, Faculty of Medicine, University of Malaya, 50603, Kuala Lumpur, Malaysia.
Vijayan MunusamyDepartment of Medicine, University of Malaya Medical Centre, 59100, Kuala Lumpur, Malaysia.
Yong Sheng LiamClinical Investigation Centre, University of Malaya Medical Centre, 59100, Kuala Lumpur, Malaysia.
Nur Husna IbrahimDepartment of Medicine, Faculty of Medicine, University of Malaya, 50603, Kuala Lumpur, Malaysia.
University Malaya Medical Centre · MYUniversity of Malaya · MY

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIn non-small cell lung cancer (NSCLC), there may be a relationship between programmed death-ligand 1 (PD-L1) expression, driver mutations and cigarette smoking.

methodsIn this single-center retrospective study, the relationship between common driver mutations (EGFR mutation and ALK rearrangement) and PD-L1 expression in advanced NSCLC according to the patients' smoking history was examined. Light, moderate and heavy smokers had smoked < 20, 20-39, and ≥ 40 pack-years, respectively. The level of PD-L1 expression, assessed using Ventana SP263 monoclonal antibody assay, was defined by the tumor proportion score (TPS) as high expression (TPS ≥ 50%), low expression (TPS 1%-49%) and no expression (TPS < 1%).

results101 (52.9%) of 191 advanced NSCLC patients were never smokers. EGFR mutations were more common in never smokers (64.4%) than in smokers (17.8%) with advanced NSCLC (P < 0.0001). A higher proportion of smokers (26.7%) had high PD-L1 expression compared to never smokers (13.9%) (P = 0.042). There was a trend for a higher proportion of male NSCLC patients [28 of 115 (24.3%)] than female patients [10 of 76 (13.2%)] to have high PD-L1 expression (P = 0.087]. High PD-L1 expression was seen in 32 of 110 (29.1%) patients with EGFR wild-type NSCLC but only in 6 of 81 (7.4%) patients with EGFR-mutant tumors (P < 0.0001). Among the 90 smokers with NSCLC, a higher proportion of heavy smokers (35.8%) than non-heavy smokers (13.5%) had high PD-L1 expression (P = 0.034). In patients with adenocarcinoma, high PD-L1 expression was seen in 25 of 77 (32.5%) patients with EGFR wild-type tumors but only in 4 of 70 (5.7%) patients with EGFR-mutant tumors (P < 0.0001). Among patients with adenocarcinoma, a significantly higher proportion of ever smokers (29.3%) than never smokers (13.5%) had high PD-L1 expression (P = 0.032). Among smokers with adenocarcinoma, a significantly higher proportion of heavy smokers (44.1%) than non-heavy smokers (8.3%) had high PD-L1 expression (P = 0.004). On multivariate analysis, after adjusting for gender and smoking status, heavy smoking and EGFR wild-type tumors remained significantly associated with high PD-L1 expression in NSCLCs and also in adenocarcinoma.

conclusionsHeavy smoking and EGFR wild-type tumors were significantly associated with high PD-L1 expression in NSCLCs and also in adenocarcinoma.

Indexed as

AdenocarcinomaCarcinoma, Non-Small-Cell LungLung NeoplasmsAnaplastic Lymphoma KinaseB7-H1 AntigenErbB ReceptorsFemaleHumansMaleMutationRetrospective StudiesSmokersAnaplastic Lymphoma KinaseB7-H1 AntigenCD274 protein, humanErbB ReceptorsEGFR mutationsNSCLCPD-L1Smoking status

Identifiers

PMID37452277
PMCPMC10347799
OpenAlexW4384340170

What OpenQuestion holds

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LicenceCC BY
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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.