{"entity": "researcher", "timestamp": "2026-08-20T21:08:47.246Z", "family": "Galanos", "given": "Panagiotis", "initials": "P", "orcid": "0000-0003-1403-4685", "affiliations": ["Genome Integrity, Danish Cancer Society Research Center, Copenhagen, Denmark."], "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/researcher/9d1071fd28cb42d6b328182cddfd341f.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/researcher/9d1071fd28cb42d6b328182cddfd341f"}}, "publications": [{"entity": "publication", "iuid": "1dddb1bd0d524404b39c4ae4dfed4ab6", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/1dddb1bd0d524404b39c4ae4dfed4ab6.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/1dddb1bd0d524404b39c4ae4dfed4ab6"}}, "title": "Hyper-recombination in ribosomal DNA is driven by long-range resection-independent RAD51 accumulation.", "authors": [{"family": "G\u00e1l", "given": "Zita", "initials": "Z"}, {"family": "Boukoura", "given": "Stavroula", "initials": "S", "orcid": "0000-0002-7176-103X", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/ebea00b102f84139835c63ec36a11326.json"}}, {"family": "Oxe", "given": "Kezia Catharina", "initials": "KC", "orcid": "0000-0002-4921-4750", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/3413af2fa0744ea49ece72eb2e709f95.json"}}, {"family": "Badawi", "given": "Sara", "initials": "S"}, {"family": "Nieto", "given": "Blanca", "initials": "B", "orcid": "0000-0001-9923-8534", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/1f92e8eb6b9d47c0bb8556ccb6beccbe.json"}}, {"family": "Korsholm", "given": "Lea Milling", "initials": "LM", "orcid": "0009-0007-9632-8957", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/98f369e2c96b4b4c89daf22d87af8cfb.json"}}, {"family": "Geisler", "given": "Sille Blangstrup", "initials": "SB", "orcid": "0009-0005-7052-9000", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/fef45bbd28a64ca3a2e8cff0de1a842a.json"}}, {"family": "Dulina", "given": "Ekaterina", "initials": "E"}, {"family": "Rasmussen", "given": "Anna Vestergaard", "initials": "AV"}, {"family": "Dahl", "given": "Christina", "initials": "C", "orcid": "0000-0002-6177-2640", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/5e2ce41bd2a346cf94e5f42150a42261.json"}}, {"family": "Lv", "given": "Wei", "initials": "W"}, {"family": "Xu", "given": "Huixin", "initials": "H"}, {"family": "Pan", "given": "Xiaoguang", "initials": "X"}, {"family": "Arampatzis", "given": "Stefanos", "initials": "S"}, {"family": "Stratou", "given": "Danai-Eleni", "initials": "DE", "orcid": "0009-0002-7380-5152", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/2b9aebe03f3c4847aa876a207b43172c.json"}}, {"family": "Galanos", "given": "Panagiotis", "initials": "P", "orcid": "0000-0003-1403-4685", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/9d1071fd28cb42d6b328182cddfd341f.json"}}, {"family": "Lin", "given": "Lin", "initials": "L", "orcid": "0000-0002-7546-4948", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/bcc1572910494eb191e316307d213606.json"}}, {"family": "Guldberg", "given": "Per", "initials": "P", "orcid": "0000-0002-4424-4803", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/321fa32fa14a4704aefb37161651bb48.json"}}, {"family": "Bartek", "given": "Jiri", "initials": "J", "orcid": "0000-0003-2013-7525", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/288939950c0c4c6393d35c84e5128b5f.json"}}, {"family": "Luo", "given": "Yonglun", "initials": "Y", "orcid": "0000-0002-0007-7759", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/f0283cb6c284428f906b0d03fda62a1e.json"}}, {"family": "Larsen", "given": "Dorthe H", "initials": "DH", "orcid": "0000-0002-8280-1252", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/f2189ec69bc54980943fe1c35084f4c8.json"}}], "type": "journal article", "published": "2024-09-06", "journal": {"title": "Nat Commun", "issn": "2041-1723", "volume": "15", "issue": "1", "pages": "7797", "issn-l": "2041-1723"}, "abstract": "Ribosomal DNA (rDNA) encodes the ribosomal RNA genes and represents an intrinsically unstable genomic region. However, the underlying mechanisms and implications for genome integrity remain elusive. Here, we use Bloom syndrome (BS), a rare genetic disease characterized by DNA repair defects and hyper-unstable rDNA, as a model to investigate the mechanisms leading to rDNA instability. We find that in Bloom helicase (BLM) proficient cells, the homologous recombination (HR) pathway in rDNA resembles that in nuclear chromatin; it is initiated by resection, replication protein A (RPA) loading and BRCA2-dependent RAD51 filament formation. However, BLM deficiency compromises RPA-loading and BRCA1/2 recruitment to rDNA, but not RAD51 accumulation. RAD51 accumulates at rDNA despite depletion of long-range resection nucleases and rDNA damage results in micronuclei when BLM is absent. In summary, our findings indicate that rDNA is permissive to RAD51 accumulation in the absence of BLM, leading to micronucleation and potentially global genomic instability.", "doi": "10.1038/s41467-024-52189-6", "pmid": "39242676", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC11379943"}, {"db": "pii", "key": "10.1038/s41467-024-52189-6"}], "notes": [], "created": "2026-08-20T08:53:38.418Z", "modified": "2026-08-20T08:53:38.808Z"}, {"entity": "publication", "iuid": "7d790256dedb49e79dd2a8f355a9f954", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/7d790256dedb49e79dd2a8f355a9f954.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/7d790256dedb49e79dd2a8f355a9f954"}}, "title": "Lamin A/C impairments cause mitochondrial dysfunction by attenuating PGC1\u03b1 and the NAMPT-NAD+ pathway.", "authors": [{"family": "Maynard", "given": "Scott", "initials": "S", "orcid": "0000-0001-5625-936X", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/608188a808184753bc3ed43e2911154c.json"}}, {"family": "Hall", "given": "Arnaldur", "initials": "A"}, {"family": "Galanos", "given": "Panagiotis", "initials": "P", "orcid": "0000-0003-1403-4685", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/9d1071fd28cb42d6b328182cddfd341f.json"}}, {"family": "Rizza", "given": "Salvatore", "initials": "S"}, {"family": "Yamamoto", "given": "Tatsuro", "initials": "T"}, {"family": "Gram", "given": "Helena Hagner", "initials": "HH"}, {"family": "Munk", "given": "Sebastian H N", "initials": "SHN"}, {"family": "Shoaib", "given": "Muhammad", "initials": "M", "orcid": "0000-0003-1296-5005", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/a90b52fbd71d432982b9807804e881f2.json"}}, {"family": "S\u00f8rensen", "given": "Claus Storgaard", "initials": "CS"}, {"family": "Bohr", "given": "Vilhelm A", "initials": "VA", "orcid": "0000-0003-4823-6429", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/57e81811b78745cc842862146c6ee7b2.json"}}, {"family": "Lerdrup", "given": "Mads", "initials": "M"}, {"family": "Maya-Mendoza", "given": "Apolinar", "initials": "A"}, {"family": "Bartek", "given": "Jiri", "initials": "J", "orcid": "0000-0003-2013-7525", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/288939950c0c4c6393d35c84e5128b5f.json"}}], "type": "journal article", "published": "2022-09-23", "journal": {"title": "Nucleic Acids Res.", "issn": "1362-4962", "volume": "50", "issue": "17", "pages": "9948-9965", "issn-l": "0305-1048"}, "abstract": "Mutations in the lamin A/C gene (LMNA) cause laminopathies such as the premature aging Hutchinson Gilford progeria syndrome (HGPS) and altered lamin A/C levels are found in diverse malignancies. The underlying lamin-associated mechanisms remain poorly understood. Here we report that lamin A/C-null mouse embryo fibroblasts (Lmna-/- MEFs) and human progerin-expressing HGPS fibroblasts both display reduced NAD+ levels, unstable mitochondrial DNA and attenuated bioenergetics. This mitochondrial dysfunction is associated with reduced chromatin recruitment (Lmna-/- MEFs) or low levels (HGPS) of PGC1\u03b1, the key transcription factor for mitochondrial homeostasis. Lmna-/- MEFs showed reduced expression of the NAD+-biosynthesis enzyme NAMPT and attenuated activity of the NAD+-dependent deacetylase SIRT1. We find high PARylation in lamin A/C-aberrant cells, further decreasing the NAD+ pool and consistent with impaired DNA base excision repair in both cell models, a condition that fuels DNA damage-induced PARylation under oxidative stress. Further, ATAC-sequencing revealed a substantially altered chromatin landscape in Lmna-/- MEFs, including aberrantly reduced accessibility at the Nampt gene promoter. Thus, we identified a new role of lamin A/C as a key modulator of mitochondrial function through impairments of PGC1\u03b1 and the NAMPT-NAD+ pathway, with broader implications for the aging process.", "doi": "10.1093/nar/gkac741", "pmid": "36099415", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC9508839"}, {"db": "pii", "key": "6696852"}], "notes": [], "created": "2026-08-20T09:49:53.952Z", "modified": "2026-08-20T09:49:54.099Z"}, {"entity": "publication", "iuid": "3350a4ecba3048d8a01a1780046ae17a", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/3350a4ecba3048d8a01a1780046ae17a.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/3350a4ecba3048d8a01a1780046ae17a"}}, "title": "Human cytomegalovirus hijacks host stress response fueling replication stress and genome instability.", "authors": [{"family": "Merchut-Maya", "given": "Joanna Maria", "initials": "JM"}, {"family": "Bartek", "given": "Jiri", "initials": "J"}, {"family": "Bartkova", "given": "Jirina", "initials": "J"}, {"family": "Galanos", "given": "Panagiotis", "initials": "P", "orcid": "0000-0003-1403-4685", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/9d1071fd28cb42d6b328182cddfd341f.json"}}, {"family": "Pantalone", "given": "Mattia Russel", "initials": "MR", "orcid": "0000-0002-2706-4683", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/ec002c989634427fb962892d402972c9.json"}}, {"family": "Lee", "given": "MyungHee", "initials": "M"}, {"family": "Cui", "given": "Huanhuan L", "initials": "HL"}, {"family": "Shilling", "given": "Patrick J", "initials": "PJ"}, {"family": "Br\u00f8chner", "given": "Christian Beltoft", "initials": "CB"}, {"family": "Broholm", "given": "Helle", "initials": "H"}, {"family": "Maya-Mendoza", "given": "Apolinar", "initials": "A", "orcid": "0000-0001-7452-9896", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/8120d9952114478b9909d9906e0dd543.json"}}, {"family": "S\u00f6derberg-Naucler", "given": "Cecilia", "initials": "C", "orcid": "0000-0001-8955-3610", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/ef2ba2f309064cddae2548ffa1b84145.json"}}], "type": "journal article", "published": "2022-08-00", "journal": {"title": "Cell Death Differ.", "issn": "1476-5403", "volume": "29", "issue": "8", "pages": "1639-1653", "issn-l": "1350-9047"}, "abstract": "Viral infections enhance cancer risk and threaten host genome integrity. Although human cytomegalovirus (HCMV) proteins have been detected in a wide spectrum of human malignancies and HCMV infections have been implicated in tumorigenesis, the underlying mechanisms remain poorly understood. Here, we employed a range of experimental approaches, including single-molecule DNA fiber analysis, and showed that infection by any of the four commonly used HCMV strains: AD169, Towne, TB40E or VR1814 induced replication stress (RS), as documented by host-cell replication fork asymmetry and formation of 53BP1 foci. The HCMV-evoked RS triggered an ensuing host DNA damage response (DDR) and chromosomal instability in both permissive and non-permissive human cells, the latter being particularly relevant in the context of tumorigenesis, as such cells can survive and proliferate after HCMV infection. The viral major immediate early enhancer and promoter (MIEP) that controls expression of the viral genes IE72 (IE-1) and IE86 (IE-2), contains transcription-factor binding sites shared by promoters of cellular stress-response genes. We found that DNA damaging insults, including those relevant for cancer therapy, enhanced IE72/86 expression. Thus, MIEP has been evolutionary shaped to exploit host DDR. Ectopically expressed IE72 and IE86 also induced RS and increased genomic instability. Of clinical relevance, we show that undergoing standard-of-care genotoxic radio-chemotherapy in patients with HCMV-positive glioblastomas correlated with elevated HCMV protein markers after tumor recurrence. Collectively, these results are consistent with our proposed concept of HCMV hijacking transcription-factor binding sites shared with host stress-response genes. We present a model to explain the potential oncomodulatory effects of HCMV infections through enhanced replication stress, subverted DNA damage response and induced genomic instability.", "doi": "10.1038/s41418-022-00953-w", "pmid": "35194187", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC9346009"}, {"db": "pii", "key": "10.1038/s41418-022-00953-w"}, {"db": "ClinicalTrials.gov", "key": "NCT04116411"}], "notes": [], "created": "2026-08-20T08:49:23.671Z", "modified": "2026-08-20T08:49:23.870Z"}, {"entity": "publication", "iuid": "12a923d86f454f0da28ae57d3a170b0d", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/12a923d86f454f0da28ae57d3a170b0d.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/12a923d86f454f0da28ae57d3a170b0d"}}, "title": "Induction of APOBEC3 Exacerbates DNA Replication Stress and Chromosomal Instability in Early Breast and Lung Cancer Evolution.", "authors": [{"family": "Venkatesan", "given": "Subramanian", "initials": "S", "orcid": "0000-0001-6454-8508", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/ecacc5d56e504429823daac1d5ea2aeb.json"}}, {"family": "Angelova", "given": "Mihaela", "initials": "M", "orcid": "0000-0002-0495-9695", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/d2d1d07f07b24def81b4d5ee64b6c60a.json"}}, {"family": "Puttick", "given": "Clare", "initials": "C"}, {"family": "Zhai", "given": "Haoran", "initials": "H"}, {"family": "Caswell", "given": "Deborah R", "initials": "DR", "orcid": "0000-0002-7550-5092", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/225c5bd5807a44398be2cce8dcc25b52.json"}}, {"family": "Lu", "given": "Wei-Ting", "initials": "WT", "orcid": "0000-0002-1405-4806", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/8acbe8b1a0394c668ccf21845b0b673e.json"}}, {"family": "Dietzen", "given": "Michelle", "initials": "M", "orcid": "0000-0002-6853-7563", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/4408177a45c844b58fb9ea4f7538d9b9.json"}}, {"family": "Galanos", "given": "Panagiotis", "initials": "P", "orcid": "0000-0003-1403-4685", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/9d1071fd28cb42d6b328182cddfd341f.json"}}, {"family": "Evangelou", "given": "Konstantinos", "initials": "K"}, {"family": "Bellelli", "given": "Roberto", "initials": "R"}, {"family": "Lim", "given": "Emilia L", "initials": "EL"}, {"family": "Watkins", "given": "Thomas B K", "initials": "TBK"}, {"family": "Rowan", "given": "Andrew", "initials": "A"}, {"family": "Teixeira", "given": "Vitor H", "initials": "VH"}, {"family": "Zhao", "given": "Yue", "initials": "Y"}, {"family": "Chen", "given": "Haiquan", "initials": "H", "orcid": "0000-0003-1689-0549", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/cdc6fa9477f94f12a85b5034d7728fff.json"}}, {"family": "Ngo", "given": "Bryan", "initials": "B"}, {"family": "Zalmas", "given": "Lykourgos-Panagiotis", "initials": "LP", "orcid": "0000-0002-4317-7709", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/e669bc02b2544f9cb61ac71d69f91a81.json"}}, {"family": "Al Bakir", "given": "Maise", "initials": "M"}, {"family": "Hobor", "given": "Sebastijan", "initials": "S"}, {"family": "Gr\u00f6nroos", "given": "Eva", "initials": "E", "orcid": "0000-0001-8303-5409", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/1fa0868fdf094f1da9bd53d4ea2b0b5d.json"}}, {"family": "Pennycuick", "given": "Adam", "initials": "A", "orcid": "0000-0001-5836-0250", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/f4eb0288b96e4807b1b119c754b7aca1.json"}}, {"family": "Nigro", "given": "Ersilia", "initials": "E"}, {"family": "Campbell", "given": "Brittany B", "initials": "BB"}, {"family": "Brown", "given": "William L", "initials": "WL", "orcid": "0000-0001-5354-9468", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/624b4fe15f824b74879cf42fa268e513.json"}}, {"family": "Akarca", "given": "Ayse U", "initials": "AU", "orcid": "0000-0003-0629-3927", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/bef78ecdb9fc4468bc0ffdbf923662e0.json"}}, {"family": "Marafioti", "given": "Teresa", "initials": "T", "orcid": "0000-0003-1223-6275", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/8b9e1588b9284cdeb7e70851280c0d6b.json"}}, {"family": "Wu", "given": "Mary Y", "initials": "MY", "orcid": "0000-0002-2074-6171", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/3230e045491e4089b405c8eddba57e12.json"}}, {"family": "Howell", "given": "Michael", "initials": "M", "orcid": "0000-0003-0912-0079", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/111f5b9b742640e5b51e15b8b0873a95.json"}}, {"family": "Boulton", "given": "Simon J", "initials": "SJ", "orcid": "0000-0002-1125-8977", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/54b9e78ef54347b39a8dd5ec4323837d.json"}}, {"family": "Bertoli", "given": "Cosetta", "initials": "C"}, {"family": "Fenton", "given": "Tim R", "initials": "TR", "orcid": "0000-0002-4737-8233", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/ea5c50a61a3747b99fd706c00ab6bafe.json"}}, {"family": "de Bruin", "given": "Robertus A M", "initials": "RAM", "orcid": "0000-0001-9957-1409", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/50a1997f1625452b862d9ecaf48f3036.json"}}, {"family": "Maya-Mendoza", "given": "Apolinar", "initials": "A", "orcid": "0000-0001-7452-9896", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/8120d9952114478b9909d9906e0dd543.json"}}, {"family": "Santoni-Rugiu", "given": "Eric", "initials": "E", "orcid": "0000-0002-2283-3535", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/36e80a5162c54a45a4b4e26b4508175d.json"}}, {"family": "Hynds", "given": "Robert E", "initials": "RE", "orcid": "0000-0002-2170-8791", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/d363c63598224cb0bd24dffc46d0d3eb.json"}}, {"family": "Gorgoulis", "given": "Vassilis G", "initials": "VG", "orcid": "0000-0001-9001-4112", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/4f7462e5c510438485b3fa91671db801.json"}}, {"family": "Jamal-Hanjani", "given": "Mariam", "initials": "M"}, {"family": "McGranahan", "given": "Nicholas", "initials": "N"}, {"family": "Harris", "given": "Reuben S", "initials": "RS"}, {"family": "Janes", "given": "Sam M", "initials": "SM", "orcid": "0000-0002-6634-5939", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/310b5ae62b03414d8cc9169b827057c6.json"}}, {"family": "Bartkova", "given": "Jirina", "initials": "J"}, {"family": "Bakhoum", "given": "Samuel F", "initials": "SF"}, {"family": "Bartek", "given": "Jiri", "initials": "J"}, {"family": "Kanu", "given": "Nnennaya", "initials": "N"}, {"family": "Swanton", "given": "Charles", "initials": "C", "orcid": "0000-0002-4299-3018", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/e624db9004da4812a607b34b20cea0e7.json"}}, {"family": "TRACERx Consortium", "given": "", "initials": ""}], "type": "journal article", "published": "2021-10-00", "journal": {"title": "Cancer Discov", "issn": "2159-8290", "volume": "11", "issue": "10", "pages": "2456-2473", "issn-l": "2159-8274"}, "abstract": "APOBEC3 enzymes are cytosine deaminases implicated in cancer. Precisely when APOBEC3 expression is induced during cancer development remains to be defined. Here we show that specific APOBEC3 genes are upregulated in breast ductal carcinoma in situ, and in preinvasive lung cancer lesions coincident with cellular proliferation. We observe evidence of APOBEC3-mediated subclonal mutagenesis propagated from TRACERx preinvasive to invasive non-small cell lung cancer (NSCLC) lesions. We find that APOBEC3B exacerbates DNA replication stress and chromosomal instability through incomplete replication of genomic DNA, manifested by accumulation of mitotic ultrafine bridges and 53BP1 nuclear bodies in the G1 phase of the cell cycle. Analysis of TRACERx NSCLC clinical samples and mouse lung cancer models revealed APOBEC3B expression driving replication stress and chromosome missegregation. We propose that APOBEC3 is functionally implicated in the onset of chromosomal instability and somatic mutational heterogeneity in preinvasive disease, providing fuel for selection early in cancer evolution. SIGNIFICANCE: This study reveals the dynamics and drivers of APOBEC3 gene expression in preinvasive disease and the exacerbation of cellular diversity by APOBEC3B through DNA replication stress to promote chromosomal instability early in cancer evolution.This article is highlighted in the In This Issue feature, p. 2355.", "doi": "10.1158/2159-8290.CD-20-0725", "pmid": "33947663", "labels": [], "xrefs": [{"db": "mid", "key": "NIHMS1710791"}, {"db": "pmc", "key": "PMC8487921"}, {"db": "pii", "key": "2159-8290.CD-20-0725"}], "notes": [], "created": "2026-08-20T12:14:28.881Z", "modified": "2026-08-20T12:14:29.593Z"}]}