Evidence map›Paper›PMID 32323836›Full record

ArticleOncology reports2020

Integrated analysis of the E2F transcription factors across cancer types.

Haiwei Wang, Xinrui Wang, Liangpu Xu, Ji Zhang, Hua Cao

Open access · hybridAbstract read
In one paragraph

Article in Oncology reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

29 citing papers in PubMed, 37 citations in OpenAlex.

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  7. The E2F family: a ray of dawn in cardiomyopathy.Molecular and cellular biochemistry · 2025
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  12. Overexpression ofTranslational lung cancer research · 2023
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  13. miR-125b-5p, miR-155-3p, and miR-214-5p and TargetInternational journal of molecular sciences · 2023
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Emerging Roles of NANOS RNA-Binding Proteins in Cancer.International journal of molecular sciences · 2022
    Article
  19. Translational cancer research · 2022
    Article
  20. Article
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

5 authors at 2 institutions in 1 country.

Haiwei WangFujian Provincial Prenatal Diagnosis Center, Fujian Provincial Maternity and Children's Hospital, Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian 350001, P.R. China.
Xinrui WangFujian Provincial Prenatal Diagnosis Center, Fujian Provincial Maternity and Children's Hospital, Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian 350001, P.R. China.
Liangpu XuFujian Provincial Prenatal Diagnosis Center, Fujian Provincial Maternity and Children's Hospital, Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian 350001, P.R. China.
Ji ZhangState Key Laboratory for Medical Genomics, Shanghai Institute of Hematology, Rui‑Jin Hospital Affiliated to School of Medicine, Shanghai Jiao Tong University, Shanghai 200025, P.R. China.
Hua CaoFujian Provincial Prenatal Diagnosis Center, Fujian Provincial Maternity and Children's Hospital, Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian 350001, P.R. China.
Fujian Medical University · CNShanghai Institute of Hematology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

E2F transcription factors are associated with the development of cancer. However, the E2F family genes have not yet been studied in a comprehensive manner. Using The Cancer Genome Atlas, the present study analyzed the functions of the E2F family genes across different types of tumor. It was revealed that compared with normal tissues, the E2F family genes are highly expressed in several types of tumor tissue. Furthermore, E2F transcription factors were significantly enriched in tumor samples across different types of tumor. The high expression levels of E2F family genes were associated with an unfavorable prognosis in liver hepatocellular carcinoma (LIHC) and lung adenocarcinoma (LUAD). Furthermore, patients with pathological T1 stage and iCluster2 molecular subtype of LIHC expressed particularly low levels of E2F family genes. The present study demonstrated that hypo‑DNA methylation, DNA amplification and TP53 mutation contributed to the high expression levels of E2F family genes in cancer cells. Finally, the present study revealed that, compared with other types of tumor, the E2F family genes were specifically downregulated in patients with LIHC. The expression levels and prognostic effects of the E2F family genes were validated using the Gene Expression Omnibus database. The results of the present study revealed the biological functions of E2F family genes in the development of cancer and provided potential biomarkers for further therapeutic studies, particularly for patients with LIHC and LUAD.

Indexed as

Gene Expression Regulation, NeoplasticBiomarkers, TumorComputational BiologyDatabases, GeneticDNA MethylationE2F Transcription FactorsGene AmplificationGene Expression ProfilingHumansNeoplasmsPrognosisSurvival RateTumor Suppressor Protein p53Biomarkers, TumorE2F Transcription FactorsTP53 protein, humanTumor Suppressor Protein p53E2F transcription factorsliver hepatocellular carcinomalung adenocarcinomapan-cancerThe Cancer Genome Atlas

Identifiers

PMID32323836
PMCPMC7058048
OpenAlexW3006014682

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.