Evidence map›Paper›PMID 36759392›Full record

ArticleJournal of cancer research and clinical oncology2023

Common inherited variants of PDCD1, CD274 and HAVCR2 genes differentially modulate the risk and prognosis of adenocarcinoma and squamous cell carcinoma.

Nafeesa Moksud, Marta Wagner, Konrad Pawełczyk, Irena Porębska, Beata Muszczyńska-Bernhard, Aneta Kowal, Andrzej Wiśniewski, Monika Kosacka, Julia Kończak, Paweł Karpiński and 5 more

Open access · hybridAbstract read
In one paragraph

Article in Journal of cancer research and clinical oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

5 citing papers in PubMed, 9 citations in OpenAlex.

  1. Cis-Regulation of an mAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 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

15 authors at 3 institutions in 1 country.

Nafeesa MoksudLaboratory of Genetics and Epigenetics of Human Diseases, Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Rudolfa Weigla 12, 53-114, Wrocław, Poland.ORCID http://orcid.org/0000-0001-8467-2661
Marta WagnerLaboratory of Genetics and Epigenetics of Human Diseases, Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Rudolfa Weigla 12, 53-114, Wrocław, Poland.ORCID http://orcid.org/0000-0002-2710-2301
Konrad PawełczykLower Silesian Centre of Oncology, Pulmonology and Heamatology, Wrocław, Poland.ORCID http://orcid.org/0000-0001-8275-7266
Irena PorębskaDepartment of Pulmonology and Lung Oncology, Wroclaw Medical University, Wrocław, Poland.ORCID http://orcid.org/0000-0001-9925-3355
Beata Muszczyńska-BernhardLower Silesian Centre of Oncology, Pulmonology and Heamatology, Wrocław, Poland.
Aneta KowalLower Silesian Centre of Oncology, Pulmonology and Heamatology, Wrocław, Poland.ORCID http://orcid.org/0000-0002-5785-2330
Andrzej WiśniewskiLaboratory of Immunogenetics and Tissue Immunology, Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Wrocław, Poland.ORCID http://orcid.org/0000-0002-1919-2298
Monika KosackaDepartment of Pulmonology and Lung Oncology, Wroclaw Medical University, Wrocław, Poland.ORCID http://orcid.org/0000-0002-5155-8886
Julia KończakDepartment of Genetics and Cell Physiology, University of Wroclaw, Wrocław, Poland.ORCID http://orcid.org/0000-0001-8621-2319
Paweł KarpińskiDepartment of Genetics, Wroclaw Medical University, Wrocław, Poland.ORCID http://orcid.org/0000-0003-3885-694X
Dominik FrydrykDepartment of Genetics and Cell Physiology, University of Wroclaw, Wrocław, Poland.
Anna AndrzejczakLaboratory of Genetics and Epigenetics of Human Diseases, Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Rudolfa Weigla 12, 53-114, Wrocław, Poland.ORCID http://orcid.org/0000-0001-6098-7554
Lidia KarabonLaboratory of Genetics and Epigenetics of Human Diseases, Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Rudolfa Weigla 12, 53-114, Wrocław, Poland.ORCID http://orcid.org/0000-0001-8172-0971
Piotr KuśnierczykLaboratory of Immunogenetics and Tissue Immunology, Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Wrocław, Poland.ORCID http://orcid.org/0000-0002-9224-8921
Monika JasekLaboratory of Genetics and Epigenetics of Human Diseases, Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Rudolfa Weigla 12, 53-114, Wrocław, Poland. monika.jasek@hirszfeld.pl.ORCID http://orcid.org/0000-0001-6778-2615
Ludwik Hirszfeld Institute of Immunology and Experimental Therapy · PLWroclaw Medical University · PLUniversity of Wrocław · PL

Funding

National Science Centre, Poland 2019/33/B/NZ5/03029
6 · The paper itself

Abstract

backgroundTo investigate the association between single nucleotide polymorphisms (SNPs) of PDCD1, CD274, and HAVCR2 genes with the risk and outcomes of non-small cell lung cancer (NSCLC) subtypes: squamous cell lung cancer (LUSC) and lung adenocarcinoma (LUAD).

methodsTaqMan SNP genotyping assays or polymerase chain reaction-restriction fragment length polymorphism methods were used to determine genotypes of: PDCD1: rs36084323, rs7421861, rs11568821, rs2227981, rs10204525; CD274: rs822335, rs10815225, rs17718883, rs2297136, rs4742098, rs4143815; HAVCR2: rs10057302, rs1036199. Among 383 NSCLC patients, 112 were diagnosed with LUAD and 116 with LUSC. The control group consisted of 433 unrelated, cancer-free subjects.

resultsA CC genotype of rs4143815 and GG genotype of rs4742098 were associated with two times higher risk of developing LUSC (CC vs. GG + GC, OR = 2.31; 95% CI = 1.32, 4.06; P = 0.003; GG vs. AA + AG, OR = 2.26; 95% CI = 1.17, 4.36; P = 0.016, respectively). Moreover, rs4143815 was an independent predictor of the age at diagnosis of LUAD. The carriers of C allele were diagnosed 4.81 years later (95% CI = 1.47, 8.15; P = 0.006) than patients with the GG genotype. The rs10057302 CA genotype was an independent predictor of overall survival in LUSC (adjusted HR = 0.13; 95% CI = 0.02, 0.93; P = 0.043). NSCLC carriers of rs11568821 T allele had almost double the risk of death (adjusted HR = 2.05; 95% CI = 1.28, 3.29; P = 0.003) compared to carriers of CC genotype.

conclusionsOur results provided additional evidence that SNPs of genes for PD-1, PD-L1 and TIM-3 differentially modulate the risk and prognosis of LUSC and LUAD.

Indexed as

AdenocarcinomaAdenocarcinoma of LungCarcinoma, Non-Small-Cell LungCarcinoma, Squamous CellLung NeoplasmsB7-H1 AntigenGenetic Predisposition to DiseaseHepatitis A Virus Cellular Receptor 2HumansPolymorphism, Single NucleotidePrognosisProgrammed Cell Death 1 ReceptorB7-H1 AntigenCD274 protein, humanHAVCR2 protein, humanHepatitis A Virus Cellular Receptor 2PDCD1 protein, humanProgrammed Cell Death 1 ReceptorCD274HAVCR2NSCLCPDCD1SNPs

Identifiers

PMID36759392
PMCPMC10356891
OpenAlexW4319827609

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.