Evidence map›Paper›PMID 25913416›Full record

ArticleBreast cancer research and treatment2015

Genome-wide analysis of alternative transcripts in human breast cancer.

Ji Wen, Kevin H Toomer, Zhibin Chen, Xiaodong Cai

Open access · greenAbstract read
In one paragraph

Article in Breast cancer research and treatment, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

24 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
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  3. Article
  4. Review
  5. Article
  6. Review
  7. PTBP1 as a potential regulator of disease.Molecular and cellular biochemistry · 2024
    Review
  8. Article
  9. Article
  10. T-Cell Intracellular Antigen 1-Like Protein in Physiology and Pathology.International journal of molecular sciences · 2022
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. RNA-binding protein KHSRP promotes tumor growth and metastasis in non-small cell lung cancer.Journal of experimental & clinical cancer research : CR · 2019
    Article
  20. Review
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

4 authors at 2 institutions in 1 country.

Ji WenDepartment of Electrical and Computer Engineering, University of Miami, 1251 Memorial Dr, EB406, Coral Gables, FL, 33146, USA.
Kevin H Toomer
Zhibin Chen
Xiaodong Cai
University of Miami · USCollege of Business and Technology · US

Funding

Sparse Structural Equation Models for Gene Networks and Chemical GenomicsR01GM104975 · NIGMS · UNIVERSITY OF MIAMI CORAL GABLES · PI CAI, XIAODONG · 2012 to 2016
$1.8M
Role of Th1/17 in gastric tumor initiation triggered by CTLA4 dysregulationR21CA178675 · NCI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI CHEN, ZHIBIN · 2013 to 2014
$360k
NCI NIH HHS R21 CA178675NCI NIH HHS R21CA178675NIGMS NIH HHS R01 GM104975NIGMS NIH HHS R01GM104975
6 · The paper itself

Abstract

Transcript variants play a critical role in diversifying gene expression. Alternative splicing is a major mechanism for generating transcript variants. A number of genes have been implicated in breast cancer pathogenesis with their aberrant expression of alternative transcripts. In this study, we performed genome-wide analyses of transcript variant expression in breast cancer. With RNA-Seq data from 105 patients, we characterized the transcriptome of breast tumors, by pairwise comparison of gene expression in the breast tumor versus matched healthy tissue from each patient. We identified 2839 genes, ~10 % of protein-coding genes in the human genome, that had differential expression of transcript variants between tumors and healthy tissues. The validity of the computational analysis was confirmed by quantitative RT-PCR assessment of transcript variant expression from four top candidate genes. The alternative transcript profiling led to classification of breast cancer into two subgroups and yielded a novel molecular signature that could be prognostic of patients' tumor burden and survival. We uncovered nine splicing factors (FOX2, MBNL1, QKI, PTBP1, ELAVL1, HNRNPC, KHDRBS1, SFRS2, and TIAR) that were involved in aberrant splicing in breast cancer. Network analyses for the coordinative patterns of transcript variant expression identified twelve "hub" genes that differentiated the cancerous and normal transcriptomes. Dysregulated expression of alternative transcripts may reveal novel biomarkers for tumor development. It may also suggest new therapeutic targets, such as the "hub" genes identified through the network analyses of transcript variant expression, or splicing factors implicated in the formation of the tumor transcriptome.

Indexed as

Alternative SplicingGene Expression Regulation, NeoplasticGenome-Wide Association StudyTranscription, GeneticBase SequenceBreast NeoplasmsCell Line, TumorCluster AnalysisComputational BiologyDatabases, Nucleic AcidFemaleGene Expression ProfilingHigh-Throughput Nucleotide SequencingHumansMolecular Sequence AnnotationNucleotide MotifsRNA-Binding Proteins

Identifiers

PMID25913416
PMCPMC5070939
OpenAlexW2086436509

What OpenQuestion holds

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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.