Evidence map›Paper›PMID 33750346›Full record

ArticleBMC cancer2021

Multi-omics analysis of genomics, epigenomics and transcriptomics for molecular subtypes and core genes for lung adenocarcinoma.

Yue Zhao, Yakun Gao, Xiaodong Xu, Jiwu Zhou, He Wang

RetractedAbstract readRetracted Publication
In one paragraph

Article in BMC cancer, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

20 citing papers in PubMed.

  1. Article
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  6. Article
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  15. Lung Cancer Computational Biology and Resources.Cold Spring Harbor perspectives in medicine · 2022
    Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Integration strategies of multi-omics data for machine learning analysis.Computational and structural biotechnology journal · 2021
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors.

Yue ZhaoDepartment II of Radiotherapy, Cangzhou Central Hospital, No.16 Xinhua West Road, Cangzhou, 061110, Hebei, China. drzhaoyue2019@163.com.
Yakun GaoDepartment of Ultrasound, Cangzhou Central Hospital, Cangzhou, 061110, Hebei, China.
Xiaodong XuSchool of Clinical Medicine, Cangzhou Medical College, Cangzhou, 061001, Hebei, China.
Jiwu ZhouDepartment II of Radiotherapy, Cangzhou Central Hospital, No.16 Xinhua West Road, Cangzhou, 061110, Hebei, China.
He WangOffice of Educational Administration, Hebei Medical University, No.361 Zhongshan East Road, Shijiazhuang, 050017, Hebei, China. wanghe@hebmu.edu.cn.ORCID http://orcid.org/0000-0002-8299-7515

Funding

Scientific Research Fund Project of Hebei Provincial Health and Family Planning Commission 20180691
6 · The paper itself

Abstract

backgroundLung adenocarcinoma (LUAD) is the most frequently diagnosed histological subtype of lung cancer. Our purpose was to explore molecular subtypes and core genes for LUAD using multi-omics analysis.

methodsMethylation, transcriptome, copy number variation (CNV), mutations and clinical feature information concerning LUAD were retrieved from The Cancer Genome Atlas Database (TCGA). Molecular subtypes were conducted via the "iClusterPlus" package in R, followed by Kaplan-Meier survival analysis. Correlation between iCluster subtypes and immune cells was analyzed. Core genes were screened out by integration of methylation, CNV and gene expression, which were externally validated by independent datasets.

resultsTwo iCluster subtypes were conducted for LUAD. Patients in imprinting centre 1 (iC1) subtype had a poorer prognosis than those in iC2 subtype. Furthermore, iC2 subtype had a higher level of B cell infiltration than iC1 subtype. Two core genes including CNTN4 and RFTN1 were screened out, both of which had higher expression levels in iC2 subtype than iC1 subtype. There were distinct differences in CNV and methylation of them between two subtypes. After validation, low expression of CNTN4 and RFTN1 predicted poorer clinical outcomes for LUAD patients.

conclusionOur findings comprehensively analyzed genomics, epigenomics, and transcriptomics of LUAD, offering novel underlying molecular mechanisms for LUAD. Two multi-omics-based core genes (CNTN4 and RFTN1) could become potential therapeutic targets for LUAD.

Indexed as

EpigenomicsTranscriptomeA549 CellsAdenocarcinoma of LungAgedContactinsDNA Copy Number VariationsDNA MethylationFemaleHumansLung NeoplasmsMaleMembrane ProteinsMiddle AgedPolymorphism, Single NucleotidePrognosisCNTN4 protein, humanContactinsMembrane ProteinsRFTN1 protein, humanCopy number variationLung adenocarcinomaMethylationMulti-omicsPrognosisSubtype

Identifiers

PMID33750346
PMCPMC7942004

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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.