{"entity": "researcher", "timestamp": "2026-09-26T14:40:50.418Z", "family": "Walter", "given": "David", "initials": "D", "orcid": "0000-0003-4363-0339", "affiliations": ["Biotech Research and Innovation Centre (BRIC), University of Copenhagen, Ole Maaloes Vej 5, Copenhagen DK-2200, Denmark."], "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/researcher/1a7abf501e364d78ab77560002fd1bad.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/researcher/1a7abf501e364d78ab77560002fd1bad"}}, "publications": [{"entity": "publication", "iuid": "4f7fedd6fc8a419aa28b9176885c6d92", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/4f7fedd6fc8a419aa28b9176885c6d92.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/4f7fedd6fc8a419aa28b9176885c6d92"}}, "title": "Chronic p53-independent p21 expression causes genomic instability by deregulating replication licensing.", "authors": [{"family": "Galanos", "given": "Panagiotis", "initials": "P"}, {"family": "Vougas", "given": "Konstantinos", "initials": "K"}, {"family": "Walter", "given": "David", "initials": "D", "orcid": "0000-0003-4363-0339", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/1a7abf501e364d78ab77560002fd1bad.json"}}, {"family": "Polyzos", "given": "Alexander", "initials": "A"}, {"family": "Maya-Mendoza", "given": "Apolinar", "initials": "A"}, {"family": "Haagensen", "given": "Emma J", "initials": "EJ"}, {"family": "Kokkalis", "given": "Antonis", "initials": "A"}, {"family": "Roumelioti", "given": "Fani-Marlen", "initials": "FM"}, {"family": "Gagos", "given": "Sarantis", "initials": "S"}, {"family": "Tzetis", "given": "Maria", "initials": "M"}, {"family": "Canovas", "given": "Bego\u00f1a", "initials": "B"}, {"family": "Igea", "given": "Ana", "initials": "A"}, {"family": "Ahuja", "given": "Akshay K", "initials": "AK"}, {"family": "Zellweger", "given": "Ralph", "initials": "R"}, {"family": "Havaki", "given": "Sofia", "initials": "S"}, {"family": "Kanavakis", "given": "Emanuel", "initials": "E"}, {"family": "Kletsas", "given": "Dimitris", "initials": "D"}, {"family": "Roninson", "given": "Igor B", "initials": "IB"}, {"family": "Garbis", "given": "Spiros D", "initials": "SD"}, {"family": "Lopes", "given": "Massimo", "initials": "M"}, {"family": "Nebreda", "given": "Angel", "initials": "A"}, {"family": "Thanos", "given": "Dimitris", "initials": "D"}, {"family": "Blow", "given": "J Julian", "initials": "JJ", "orcid": "0000-0002-9524-5849", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/d63c5296e68a46b18c6b91f5ea53f021.json"}}, {"family": "Townsend", "given": "Paul", "initials": "P"}, {"family": "S\u00f8rensen", "given": "Claus Storgaard", "initials": "CS"}, {"family": "Bartek", "given": "Jiri", "initials": "J"}, {"family": "Gorgoulis", "given": "Vassilis G", "initials": "VG"}], "type": "journal article", "published": "2016-07-00", "journal": {"title": "Nat. Cell Biol.", "issn": "1476-4679", "volume": "18", "issue": "7", "pages": "777-789", "issn-l": "1465-7392"}, "abstract": "The cyclin-dependent kinase inhibitor p21(WAF1/CIP1) (p21) is a cell-cycle checkpoint effector and inducer of senescence, regulated by p53. Yet, evidence suggests that p21 could also be oncogenic, through a mechanism that has so far remained obscure. We report that a subset of atypical cancerous cells strongly expressing p21 showed proliferation features. This occurred predominantly in p53-mutant human cancers, suggesting p53-independent upregulation of p21 selectively in more aggressive tumour cells. Multifaceted phenotypic and genomic analyses of p21-inducible, p53-null, cancerous and near-normal cellular models showed that after an initial senescence-like phase, a subpopulation of p21-expressing proliferating cells emerged, featuring increased genomic instability, aggressiveness and chemoresistance. Mechanistically, sustained p21 accumulation inhibited mainly the CRL4-CDT2 ubiquitin ligase, leading to deregulated origin licensing and replication stress. Collectively, our data reveal the tumour-promoting ability of p21 through deregulation of DNA replication licensing machinery-an unorthodox role to be considered in cancer treatment, since p21 responds to various stimuli including some chemotherapy drugs.", "doi": "10.1038/ncb3378", "pmid": "27323328", "labels": [], "xrefs": [{"db": "mid", "key": "EMS83002"}, {"db": "pmc", "key": "PMC6535144"}, {"db": "pii", "key": "ncb3378"}], "notes": [], "created": "2018-12-05T08:55:48.993Z", "modified": "2026-09-23T06:37:44.862Z"}]}