ArticleBioinformatics (Oxford, England)2013
HMCan: a method for detecting chromatin modifications in cancer samples using ChIP-seq data.
Article in Bioinformatics (Oxford, England), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed.
- Epigenetic profiling reveals key super-enhancer networks driving oncogenesis in HPV-positive HNSCC.iScience · 2025Article
- Transforming Cancer Diagnostics: The Emergence of Liquid Biopsy and Epigenetic Markers.MedComm · 2025Review
- The Super Enhancer-Driven Long Noncoding RNA PRKCQ-AS1 Promotes Neuroblastoma Tumorigenesis by Interacting With MSI2 Protein and Is Targetable by Small Molecule Compounds.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Copy number normalization distinguishes differential signals driven by copy number differences in ATAC-seq and ChIP-seq.BMC genomics · 2025Article
- Rescuing biologically relevant consensus regions across replicated samples.BMC bioinformatics · 2023Article
- Reversible transitions between noradrenergic and mesenchymal tumor identities define cell plasticity in neuroblastoma.Nature communications · 2023Article
- MacroH2A histone variants modulate enhancer activity to repress oncogenic programs and cellular reprogramming.Communications biology · 2023Article
- Article
- HDAC1 and PRC2 mediate combinatorial control in SPI1/PU.1-dependent gene repression in murine erythroleukaemia.Nucleic acids research · 2022Article
- The Role of ARID1A in the Nonestrogenic Modulation of IGF-1 Signaling.Molecular cancer research : MCR · 2022Article
- CHIPIN: ChIP-seq inter-sample normalization based on signal invariance across transcriptionally constant genes.BMC bioinformatics · 2021Article
- CoBRA: Containerized Bioinformatics Workflow for Reproducible ChIP/ATAC-seq Analysis.Genomics, proteomics & bioinformatics · 2021Article
- HOTAIR lncRNA promotes epithelial-mesenchymal transition by redistributing LSD1 at regulatory chromatin regions.EMBO reports · 2021Article
- Increased peak detection accuracy in over-dispersed ChIP-seq data with supervised segmentation models.BMC bioinformatics · 2021Article
- Chromatin Immunoprecipitation Followed by Next-Generation Sequencing (ChIP-Seq) Analysis in Ewing Sarcoma.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Analysis of H3K4me3 and H3K27me3 bivalent promotors in HER2+ breast cancer cell lines reveals variations depending on estrogen receptor status and significantly correlates with gene expression.BMC medical genomics · 2020Article
- NR2F2 Orphan Nuclear Receptor is Involved in Estrogen Receptor Alpha-Mediated Transcriptional Regulation in Luminal A Breast Cancer Cells.International journal of molecular sciences · 2020Article
- ncHMR detector: a computational framework to systematically reveal non-classical functions of histone modification regulators.Genome biology · 2020Article
- GSK2801, a BAZ2/BRD9 Bromodomain Inhibitor, Synergizes with BET Inhibitors to Induce Apoptosis in Triple-Negative Breast Cancer.Molecular cancer research : MCR · 2019Article
- Distinct epigenetic landscapes underlie the pathobiology of pancreatic cancer subtypes.Nature communications · 2018Article
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7 authors.
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No grant is acknowledged in the PubMed record.
Abstract
motivationCancer cells are often characterized by epigenetic changes, which include aberrant histone modifications. In particular, local or regional epigenetic silencing is a common mechanism in cancer for silencing expression of tumor suppressor genes. Though several tools have been created to enable detection of histone marks in ChIP-seq data from normal samples, it is unclear whether these tools can be efficiently applied to ChIP-seq data generated from cancer samples. Indeed, cancer genomes are often characterized by frequent copy number alterations: gains and losses of large regions of chromosomal material. Copy number alterations may create a substantial statistical bias in the evaluation of histone mark signal enrichment and result in underdetection of the signal in the regions of loss and overdetection of the signal in the regions of gain.
resultsWe present HMCan (Histone modifications in cancer), a tool specially designed to analyze histone modification ChIP-seq data produced from cancer genomes. HMCan corrects for the GC-content and copy number bias and then applies Hidden Markov Models to detect the signal from the corrected data. On simulated data, HMCan outperformed several commonly used tools developed to analyze histone modification data produced from genomes without copy number alterations. HMCan also showed superior results on a ChIP-seq dataset generated for the repressive histone mark H3K27me3 in a bladder cancer cell line. HMCan predictions matched well with experimental data (qPCR validated regions) and included, for example, the previously detected H3K27me3 mark in the promoter of the DLEC1 gene, missed by other tools we tested.
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