ArticleScience (New York, N.Y.)2016
The linker histone H1.0 generates epigenetic and functional intratumor heterogeneity.
Article in Science (New York, N.Y.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers.
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Who cites it
112 citing papers in PubMed.
- Origins and consequences of oncogenic 3D chromatin remodelling.Nature reviews. Cancer · 2026Review
- Heterogeneity in cancer: molecular mechanisms and therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- Cancer stem cell plasticity: mechanisms, immune microenvironment crosstalk, and therapeutic implications.Journal of hematology & oncology · 2026Review
- Neofunctionalization of H1 linker histones drives divergent gene expression and histone methylation in Cryptococcus neoformans.Communications biology · 2026Article
- Electrical stimulation promotes longevity and regeneration in a colonial chordate.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Linker histones consolidate heterogenous nucleosome fiber contacts by linking together multiple nucleosomes.Nature communications · 2026Article
- Molecular underpinnings of induced degenerative heterogeneity in the retinal pigment epithelium.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Linker histone H1.5 contributes to centromere integrity.Nucleic acids research · 2026Article
- A chromatin fiber model explains cell-free DNA fragmentation signatures of active regulatory elements.bioRxiv : the preprint server for biology · 2025Article
- Linker histone regulates the myeloid versus lymphoid bifurcation of multipotent hematopoietic stem and progenitors.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Epitalon increases telomere length in human cell lines through telomerase upregulation or ALT activity.Biogerontology · 2025Article
- Aere perennius: how chromatin fidelity is maintained and lost in disease.NAR molecular medicine · 2025Review
- Investigation of the clinical significance of the expression of immunohistochemical biomarkers Enhancer of zeste homolog 2 and Forkhead box M1 in localized prostate cancer tissue: A Greek retrospective study.Asian journal of urology · 2025Article
- The linker histone chaperone Prothymosin α (PTMA) is essential for efficient DNA damage repair and the recruitment of PARP1.Epigenetics & chromatin · 2025Article
- H1-0 is a specific mediator of the repressive ETV6::RUNX1 transcriptional landscape in preleukemia and B cell acute lymphoblastic leukemia.HemaSphere · 2025Article
- MRI-based deep learning radiomics to differentiate dual-phenotype hepatocellular carcinoma from HCC and intrahepatic cholangiocarcinoma: a multicenter study.Insights into imaging · 2025Article
- Deregulated methylation and expression ofFrontiers in immunology · 2025Article
- Panoramic view of MDH1: driving cancer progression and shaping the tumor immune microenvironment.Frontiers in immunology · 2025Article
- The Emerging Role of ADAM 12 Regulates Epithelial-mesenchymal Transition by Activating the Wnt/β-catenin Signaling Pathway in Colorectal Cancer.Recent patents on anti-cancer drug discovery · 2025Article
- Article
52 more citing papers are in PubMed but not listed here.
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16 authors.
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Abstract
Tumors comprise functionally diverse subpopulations of cells with distinct proliferative potential. Here, we show that dynamic epigenetic states defined by the linker histone H1.0 determine which cells within a tumor can sustain the long-term cancer growth. Numerous cancer types exhibit high inter- and intratumor heterogeneity of H1.0, with H1.0 levels correlating with tumor differentiation status, patient survival, and, at the single-cell level, cancer stem cell markers. Silencing of H1.0 promotes maintenance of self-renewing cells by inducing derepression of megabase-sized gene domains harboring downstream effectors of oncogenic pathways. Self-renewing epigenetic states are not stable, and reexpression of H1.0 in subsets of tumor cells establishes transcriptional programs that restrict cancer cells' long-term proliferative potential and drive their differentiation. Our results uncover epigenetic determinants of tumor-maintaining cells.
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