Evidence map›Paper›PMID 25180182›Full record

ArticleBioMed research international2014

Novel approach for coexpression analysis of E2F1-3 and MYC target genes in chronic myelogenous leukemia.

Fengfeng Wang, Lawrence W C Chan, William C S Cho, Petrus Tang, Jun Yu, Chi-Ren Shyu, Nancy B Y Tsui, S C Cesar Wong, Parco M Siu, S P Yip and 1 more

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2014. 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
0.8field-weighted citation impact, top 28% 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, 5 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

11 authors at 5 institutions in 4 countries.

Fengfeng WangDepartment of Health Technology and Informatics, Hong Kong Polytechnic University, Lee Shau Kee Building, Hung Hom, Kowloon, Hong Kong.ORCID 0000-0003-4959-4527
Lawrence W C ChanDepartment of Health Technology and Informatics, Hong Kong Polytechnic University, Lee Shau Kee Building, Hung Hom, Kowloon, Hong Kong.ORCID 0000-0001-6451-2273
William C S ChoDepartment of Clinical Oncology, Queen Elizabeth Hospital, 30 Gascoigne Road, Kowloon, Hong Kong.
Petrus TangBioinformatics Center, Chang Gung University, Taoyuan 333, Taiwan.
Jun YuBeijing Institute of Genomics, Chinese Academy of Sciences, Chaoyang District, Beijing 100029, China.
Chi-Ren ShyuDepartment of Computer Science, Informatics Institute, University of Missouri, Columbia, MO 65211, USA.
Nancy B Y TsuiDepartment of Health Technology and Informatics, Hong Kong Polytechnic University, Lee Shau Kee Building, Hung Hom, Kowloon, Hong Kong.
S C Cesar WongDepartment of Health Technology and Informatics, Hong Kong Polytechnic University, Lee Shau Kee Building, Hung Hom, Kowloon, Hong Kong.
Parco M SiuDepartment of Health Technology and Informatics, Hong Kong Polytechnic University, Lee Shau Kee Building, Hung Hom, Kowloon, Hong Kong.
S P YipDepartment of Health Technology and Informatics, Hong Kong Polytechnic University, Lee Shau Kee Building, Hung Hom, Kowloon, Hong Kong.
Benjamin Y M YungDepartment of Health Technology and Informatics, Hong Kong Polytechnic University, Lee Shau Kee Building, Hung Hom, Kowloon, Hong Kong.
Hong Kong Polytechnic University · HKBeijing Institute of Genomics · CNChang Gung University · TWQueen Elizabeth Hospital · CNUniversity of Missouri · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundChronic myelogenous leukemia (CML) is characterized by tremendous amount of immature myeloid cells in the blood circulation. E2F1-3 and MYC are important transcription factors that form positive feedback loops by reciprocal regulation in their own transcription processes. Since genes regulated by E2F1-3 or MYC are related to cell proliferation and apoptosis, we wonder if there exists difference in the coexpression patterns of genes regulated concurrently by E2F1-3 and MYC between the normal and the CML states.

resultsWe proposed a method to explore the difference in the coexpression patterns of those candidate target genes between the normal and the CML groups. A disease-specific cutoff point for coexpression levels that classified the coexpressed gene pairs into strong and weak coexpression classes was identified. Our developed method effectively identified the coexpression pattern differences from the overall structure. Moreover, we found that genes related to the cell adhesion and angiogenesis properties were more likely to be coexpressed in the normal group when compared to the CML group.

conclusionOur findings may be helpful in exploring the underlying mechanisms of CML and provide useful information in cancer treatment.

Indexed as

Gene Expression Regulation, NeoplasticCells, CulturedE2F1 Transcription FactorE2F3 Transcription FactorGene Expression ProfilingGene TargetingHumansLeukemia, Myelogenous, Chronic, BCR-ABL PositiveNeoplasm ProteinsProto-Oncogene Proteins c-mycE2F1 protein, humanE2F1 Transcription FactorE2F3 protein, humanE2F3 Transcription FactorNeoplasm ProteinsProto-Oncogene Proteins c-myc

Identifiers

PMID25180182
PMCPMC4142389
OpenAlexW1974474223

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

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.