000266479 001__ 266479
000266479 005__ 20250127091811.0
000266479 0247_ $$2pmid$$apmid:37828086
000266479 0247_ $$2doi$$a10.1038/s41418-023-01227-9
000266479 0247_ $$2ISSN$$a1350-9047
000266479 0247_ $$2ISSN$$a1476-5403
000266479 0247_ $$2altmetric$$aaltmetric:155448153
000266479 0247_ $$2pmc$$apmc:PMC11748643
000266479 037__ $$aDZNE-2023-01164
000266479 041__ $$aEnglish
000266479 082__ $$a610
000266479 1001_ $$0P:(DE-2719)2811779$$aSalomoni, Paolo$$b0$$eFirst author
000266479 245__ $$a(B)On(e)-cohistones and the epigenetic alterations at the root of bone cancer
000266479 260__ $$aLondon$$bMacmillan$$c2025
000266479 3367_ $$2DRIVER$$aarticle
000266479 3367_ $$2DataCite$$aOutput Types/Journal article
000266479 3367_ $$0PUB:(DE-HGF)16$$2PUB:(DE-HGF)$$aJournal Article$$bjournal$$mjournal$$s1737363188_4998$$xReview Article
000266479 3367_ $$2BibTeX$$aARTICLE
000266479 3367_ $$2ORCID$$aJOURNAL_ARTICLE
000266479 3367_ $$00$$2EndNote$$aJournal Article
000266479 520__ $$aIdentification of mutations in histones in a number of human neoplasms and developmental syndromes represents the most compelling evidence to date for a causal role of epigenetic perturbations in human disease. In most cases, these mutations have gain of function properties that cause deviation from normal developmental processes leading to embryo defects and/or neoplastic transformation. These exciting discoveries represent a step-change in our understanding of the role of chromatin (dys)regulation in development and disease. However, the mechanisms of action of oncogenic histone mutations (oncohistones) remain only partially understood. Here, we critically assess existing literature on oncohistones focussing mainly on bone neoplasms. We show how it is possible to draw parallels with some of the cell-autonomous mechanisms of action described in paediatric brain cancer, although the functions of oncohistones in bone tumours remain under-investigated. In this respect, it is becoming clear that histone mutations targeting the same residues display, at least in part, tissue-specific oncogenic mechanisms. Furthermore, it is emerging that cancer cells carrying oncohistones can modify the surrounding microenvironment to support growth and/or alter differentiation trajectories. A better understanding of oncohistone function in different neoplasms provide potential for identification of signalling that could be targeted therapeutically. Finally, we discuss some of the main concepts and future directions in this research area, while also drawing possible connections and parallels with other cancer epigenetic mechanisms.
000266479 536__ $$0G:(DE-HGF)POF4-352$$a352 - Disease Mechanisms (POF4-352)$$cPOF4-352$$fPOF IV$$x0
000266479 588__ $$aDataset connected to CrossRef, Journals: pub.dzne.de
000266479 650_2 $$2MeSH$$aHumans
000266479 650_2 $$2MeSH$$aEpigenesis, Genetic
000266479 650_2 $$2MeSH$$aBone Neoplasms: genetics
000266479 650_2 $$2MeSH$$aBone Neoplasms: metabolism
000266479 650_2 $$2MeSH$$aBone Neoplasms: pathology
000266479 650_2 $$2MeSH$$aHistones: metabolism
000266479 650_2 $$2MeSH$$aMutation
000266479 650_2 $$2MeSH$$aAnimals
000266479 7001_ $$00000-0002-2832-1303$$aFlanagan, Adrienne M.$$b1
000266479 7001_ $$00000-0002-9397-4925$$aCottone, Lucia$$b2
000266479 773__ $$0PERI:(DE-600)1496681-5$$a10.1038/s41418-023-01227-9$$n1$$p66 - 77$$tCell death and differentiation$$v32$$x1350-9047$$y2025
000266479 8564_ $$uhttps://pub.dzne.de/record/266479/files/DZNE-2023-01164.pdf$$yOpenAccess
000266479 8564_ $$uhttps://pub.dzne.de/record/266479/files/DZNE-2023-01164.pdf?subformat=pdfa$$xpdfa$$yOpenAccess
000266479 909CO $$ooai:pub.dzne.de:266479$$pdnbdelivery$$pdriver$$pVDB$$popen_access$$popenaire
000266479 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)2811779$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b0$$kDZNE
000266479 9131_ $$0G:(DE-HGF)POF4-352$$1G:(DE-HGF)POF4-350$$2G:(DE-HGF)POF4-300$$3G:(DE-HGF)POF4$$4G:(DE-HGF)POF$$aDE-HGF$$bGesundheit$$lNeurodegenerative Diseases$$vDisease Mechanisms$$x0
000266479 9141_ $$y2023
000266479 915__ $$0StatID:(DE-HGF)0200$$2StatID$$aDBCoverage$$bSCOPUS$$d2023-10-21
000266479 915__ $$0StatID:(DE-HGF)0160$$2StatID$$aDBCoverage$$bEssential Science Indicators$$d2023-10-21
000266479 915__ $$0StatID:(DE-HGF)1050$$2StatID$$aDBCoverage$$bBIOSIS Previews$$d2023-10-21
000266479 915__ $$0StatID:(DE-HGF)1190$$2StatID$$aDBCoverage$$bBiological Abstracts$$d2023-10-21
000266479 915__ $$0StatID:(DE-HGF)0600$$2StatID$$aDBCoverage$$bEbsco Academic Search$$d2023-10-21
000266479 915__ $$0StatID:(DE-HGF)0100$$2StatID$$aJCR$$bCELL DEATH DIFFER : 2022$$d2023-10-21
000266479 915__ $$0StatID:(DE-HGF)1030$$2StatID$$aDBCoverage$$bCurrent Contents - Life Sciences$$d2023-10-21
000266479 915__ $$0StatID:(DE-HGF)9910$$2StatID$$aIF >= 10$$bCELL DEATH DIFFER : 2022$$d2023-10-21
000266479 915__ $$0StatID:(DE-HGF)0113$$2StatID$$aWoS$$bScience Citation Index Expanded$$d2023-10-21
000266479 915__ $$0StatID:(DE-HGF)3002$$2StatID$$aDEAL Springer$$d2023-10-21$$wger
000266479 915__ $$0StatID:(DE-HGF)0150$$2StatID$$aDBCoverage$$bWeb of Science Core Collection$$d2023-10-21
000266479 915__ $$0LIC:(DE-HGF)CCBY4$$2HGFVOC$$aCreative Commons Attribution CC BY 4.0
000266479 915__ $$0StatID:(DE-HGF)0510$$2StatID$$aOpenAccess
000266479 915__ $$0StatID:(DE-HGF)0030$$2StatID$$aPeer Review$$bASC$$d2023-10-21
000266479 915__ $$0StatID:(DE-HGF)0300$$2StatID$$aDBCoverage$$bMedline$$d2023-10-21
000266479 915__ $$0StatID:(DE-HGF)0320$$2StatID$$aDBCoverage$$bPubMed Central$$d2023-10-21
000266479 915__ $$0StatID:(DE-HGF)0199$$2StatID$$aDBCoverage$$bClarivate Analytics Master Journal List$$d2023-10-21
000266479 9201_ $$0I:(DE-2719)1013032$$kAG Salomoni$$lNuclear Function in CNS Pathophysiology$$x0
000266479 980__ $$ajournal
000266479 980__ $$aVDB
000266479 980__ $$aI:(DE-2719)1013032
000266479 980__ $$aUNRESTRICTED
000266479 9801_ $$aFullTexts