Evidence map›Paper›PMID 31429720›Full record

ArticleBMC cancer2019

Distinct signatures of lung cancer types: aberrant mucin O-glycosylation and compromised immune response.

Marta Lucchetta, Isabelle da Piedade, Mohamed Mounir, Marina Vabistsevits, Thilde Terkelsen, Elena Papaleo

Abstract read
In one paragraph

Article in BMC cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing 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

27 citing papers in PubMed.

  1. Article
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  4. Review
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  6. Article
  7. MUC21: a new target for tumor treatment.Frontiers in oncology · 2024
    Review
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  19. Article
  20. DifferentialOncology reports · 2021
    Observational
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

6 authors.

Marta LucchettaComputational Biology Laboratory, Danish Cancer Society Research Center, Strandboulevarden 49, 2100, Copenhagen, Denmark.
Isabelle da PiedadeComputational Biology Laboratory, Danish Cancer Society Research Center, Strandboulevarden 49, 2100, Copenhagen, Denmark.
Mohamed MounirComputational Biology Laboratory, Danish Cancer Society Research Center, Strandboulevarden 49, 2100, Copenhagen, Denmark.
Marina VabistsevitsComputational Biology Laboratory, Danish Cancer Society Research Center, Strandboulevarden 49, 2100, Copenhagen, Denmark.
Thilde TerkelsenComputational Biology Laboratory, Danish Cancer Society Research Center, Strandboulevarden 49, 2100, Copenhagen, Denmark.
Elena PapaleoComputational Biology Laboratory, Danish Cancer Society Research Center, Strandboulevarden 49, 2100, Copenhagen, Denmark. elenap@cancer.dk.ORCID http://orcid.org/0000-0003-2296-898X

Funding

Danmarks Grundforskningsfond DNRF125Innovationsfonden 5189-00052B
6 · The paper itself

Abstract

backgroundGenomic initiatives such as The Cancer Genome Atlas (TCGA) contain data from -omics profiling of thousands of tumor samples, which may be used to decipher cancer signaling, and related alterations. Managing and analyzing data from large-scale projects, such as TCGA, is a demanding task. It is difficult to dissect the high complexity hidden in genomic data and to account for inter-tumor heterogeneity adequately.

methodsIn this study, we used a robust statistical framework along with the integration of diverse bioinformatic tools to analyze next-generation sequencing data from more than 1000 patients from two different lung cancer subtypes, i.e., the lung adenocarcinoma (LUAD) and the squamous cell carcinoma (LUSC).

resultsWe used the gene expression data to identify co-expression modules and differentially expressed genes to discriminate between LUAD and LUSC. We identified a group of genes which could act as specific oncogenes or tumor suppressor genes in one of the two lung cancer types, along with two dual role genes. Our results have been validated against other transcriptomics data of lung cancer patients.

conclusionsOur integrative approach allowed us to identify two key features: a substantial up-regulation of genes involved in O-glycosylation of mucins in LUAD, and a compromised immune response in LUSC. The immune-profile associated with LUSC might be linked to the activation of three oncogenic pathways, which promote the evasion of the antitumor immune response. Collectively, our results provide new future directions for the design of target therapies in lung cancer.

Indexed as

Adenocarcinoma of LungCarcinoma, Squamous CellCohort StudiesDatabases, Nucleic AcidGene Expression Regulation, NeoplasticGlycosylationHumansInterleukin-6Keratins, Type ILung NeoplasmsMembrane GlycoproteinsMucin-5BMucinsMultigene FamilyProportional Hazards ModelsRNA-SeqIL6 protein, humanInterleukin-6Keratins, Type IKRT23 protein, humanMembrane GlycoproteinsMUC21 protein, humanMUC5B protein, humanMucin-5BMucinsCo-expressionDifferential expression analysisLung adenocarcinomaLung squamous cell carcinomaRNA-SeqSoft clusteringSurvival analysisTCGA

Identifiers

PMID31429720
PMCPMC6702745

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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.