{"entity": "researcher", "timestamp": "2026-08-20T20:42:17.614Z", "family": "S\u00f6derberg-Naucler", "given": "Cecilia", "initials": "C", "orcid": "0000-0001-8955-3610", "affiliations": ["Department of Medicine, Unit of Microbial Pathogenesis, Karolinska Institutet, Stockholm, Sweden. cecilia.naucler@ki.se.", "Department of Neurology, Karolinska University Hospital, Stockholm, Sweden. cecilia.naucler@ki.se.", "MediCity Research Laboratory, University of Turku, Turku, Finland. cecilia.naucler@ki.se.", "Institute of Biomedicine, University of Turku, Turku, Finland. cecilia.naucler@ki.se."], "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/researcher/ef2ba2f309064cddae2548ffa1b84145.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/researcher/ef2ba2f309064cddae2548ffa1b84145"}}, "publications": [{"entity": "publication", "iuid": "2550591caa6d45ec8f9712a56538907d", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/2550591caa6d45ec8f9712a56538907d.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/2550591caa6d45ec8f9712a56538907d"}}, "title": "Does human cytomegalovirus provide a novel therapeutic target for patients with glioblastoma?", "authors": [{"family": "S\u00f6derberg-Naucler", "given": "Cecilia", "initials": "C", "orcid": "0000-0001-8955-3610", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/ef2ba2f309064cddae2548ffa1b84145.json"}}, {"family": "Pantalone", "given": "Mattia R", "initials": "MR", "orcid": "0000-0002-2706-4683", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/ec002c989634427fb962892d402972c9.json"}}, {"family": "Stragliotto", "given": "Giuseppe", "initials": "G", "orcid": "0000-0003-1968-6447", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/2930c923f8644d7a921f6c6544fe9909.json"}}, {"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": "2025-11-06", "journal": {"title": "Philos. Trans. R. Soc. Lond., B, Biol. Sci.", "issn": "1471-2970", "volume": "380", "issue": "1938", "pages": "20240403", "issn-l": "0962-8436"}, "abstract": "Glioblastoma is the most common and aggressive primary malignant brain tumour in adults, with limited treatment options despite years of research. Since the 2005 introduction of the current standard of care, hundreds of clinical trials have failed to deliver significant breakthroughs. In 2002, human cytomegalovirus (HCMV) was detected in 100% of glioblastoma tumours. Although its role in cancer remains debated, and HCMV is not classified as an oncovirus, numerous studies have reported high viral prevalence in glioblastoma. HCMV can induce all 10 'hallmarks of cancer' and has been shown to modify both tumour cell behaviour and the microenvironment, which may enhance tumour growth and promote immune evasion. The association between HCMV and poor glioblastoma prognosis has generated increasing interest in targeting the virus therapeutically. Our clinical studies suggest that adding antiviral treatment to standard care may improve survival in both primary and recurrent glioblastoma. Moreover, an mRNA-based HCMV pp65 dendritic cell vaccine has shown preliminary indications of a potential survival benefit in early phase studies. Future research should prioritize clarifying HCMV's role in glioblastoma and rigorously evaluating antiviral and immunotherapeutic strategies in randomized clinical trials.This article is part of the theme issue 'The indirect effects of cytomegalovirus infection: mechanisms and consequences'.", "doi": "10.1098/rstb.2024.0403", "pmid": "41194660", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC12590173"}], "notes": [], "created": "2026-08-20T09:53:03.235Z", "modified": "2026-08-20T09:53:03.359Z"}, {"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"}]}