ArticleBMC genomics2012
Overrepresentation of transcription factor families in the genesets underlying breast cancer subtypes.
Article in BMC genomics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- A time-resolved multi-omics atlas of transcriptional regulation in response to high-altitude hypoxia across whole-body tissues.Nature communications · 2024Article
- Tumor-derived miR-130b-3p induces cancer-associated fibroblast activation by targeting SPIN90 in luminal A breast cancer.Oncogenesis · 2022Article
- Sample-Specific Perturbation of Gene Interactions Identifies Pancreatic Cancer Subtypes.International journal of molecular sciences · 2022Article
- Aged Callus Skeletal Stem/Progenitor Cells Contain an Inflammatory Osteogenic Population With Increased IRF and NF-κB Pathways and Reduced Osteogenic Potential.Frontiers in molecular biosciences · 2022Article
- Sample-specific perturbation of gene interactions identifies breast cancer subtypes.Briefings in bioinformatics · 2021Article
- Subtype-specific transcriptional regulators in breast tumors subjected to genetic and epigenetic alterations.Bioinformatics (Oxford, England) · 2020Article
- Removing Background Co-occurrences of Transcription Factor Binding Sites Greatly Improves the Prediction of Specific Transcription Factor Cooperations.Frontiers in genetics · 2018Article
- Nek2A/SuFu feedback loop regulates Gli-mediated Hedgehog signaling pathway.International journal of oncology · 2017Article
- PC-TraFF: identification of potentially collaborating transcription factors using pointwise mutual information.BMC bioinformatics · 2015Article
- Article
- Complex-based analysis of dysregulated cellular processes in cancer.BMC systems biology · 2014Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe human genome contains a large amount of cis-regulatory DNA elements responsible for directing both spatial and temporal gene-expression patterns. Previous studies have shown that based on their mRNA expression breast tumors could be divided into five subgroups (Luminal A, Luminal B, Basal, ErbB2(+) and Normal-like), each with a distinct molecular portrait. Whole genome gene expression analysis of independent sets of breast tumors reveals repeatedly the robustness of this classification. Furthermore, breast tumors carrying a TP53 mutation show a distinct gene expression profile, which is in strong association to the distinct molecular portraits. The mRNA expression of 552 genes, which varied considerably among the different tumors, but little between two samples of the same tumor, has been shown to be sufficient to separate these tumor subgroups.
resultsWe analyzed in silico the transcriptional regulation of genes defining the subgroups at 3 different levels: 1. We studied the pathways in which the genes distinguishing the subgroups of breast cancer may be jointly involved including upstream regulators (1st and 2nd level of regulation) as well as downstream targets of these genes. 2. Then we analyzed the promoter areas of these genes (-500 bp tp +100 bp relative to the transcription start site) for canonical transcription binding sites using Genomatix. 3. We looked for the actual expression levels of the identified TF and how they correlate with the overrepresentation of their TF binding sites in the separate groups. We report that promoter composition of the genes that most strongly predict the patient subgroups is distinct. The class-predictive genes showed a clearly different degree of overrepresentation of transcription factor families in their promoter sequences.
conclusionThe study suggests that transcription factors responsible for the observed expression pattern in breast cancers may lead us to important biological pathways.
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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.