{"entity": "researcher", "timestamp": "2026-07-12T09:08:04.630Z", "family": "Leandersson", "given": "Karin", "initials": "K", "orcid": "0000-0001-8254-3137", "affiliations": ["1Cancer Immunology, Department of Translational Medicine, Lund University, Malm\u00f6, 21428 Sweden."], "links": {"self": {"href": "https://publications.scilifelab.se/researcher/4736923f382845c2990efb251340bfb4.json"}, "display": {"href": "https://publications.scilifelab.se/researcher/4736923f382845c2990efb251340bfb4"}}, "publications": [{"entity": "publication", "iuid": "5030ff3ac322493db0bee8969ebf9d14", "links": {"self": {"href": "https://publications.scilifelab.se/publication/5030ff3ac322493db0bee8969ebf9d14.json"}, "display": {"href": "https://publications.scilifelab.se/publication/5030ff3ac322493db0bee8969ebf9d14"}}, "title": "Reliable on-treatment prognostication and target identification with a customized assay for circulating tumor DNA in patients with newly diagnosed pancreatic cancer.", "authors": [{"family": "Petersson", "given": "Alexandra", "initials": "A", "orcid": "0000-0002-5574-9217", "researcher": {"href": "https://publications.scilifelab.se/researcher/98f02e97bd25493c993d1a2568935885.json"}}, {"family": "Svensson", "given": "Maja", "initials": "M"}, {"family": "Hau", "given": "Sofie Olsson", "initials": "SO"}, {"family": "Bergstr\u00f6m", "given": "Rebecka", "initials": "R", "orcid": "0000-0001-7609-0733", "researcher": {"href": "https://publications.scilifelab.se/researcher/9c52bb8b2ae249049f0da222bcdfe932.json"}}, {"family": "Lindberg", "given": "Johan", "initials": "J", "orcid": "0000-0003-3610-6774", "researcher": {"href": "https://publications.scilifelab.se/researcher/1369ca149def47a8abb8abb90b23ca66.json"}}, {"family": "Mayrhofer", "given": "Markus", "initials": "M"}, {"family": "Chattopadhyay", "given": "Subhayan", "initials": "S", "orcid": "0000-0002-8599-2971", "researcher": {"href": "https://publications.scilifelab.se/researcher/78358668578b4661bed1f6a37365fae4.json"}}, {"family": "Eberhard", "given": "Jakob", "initials": "J"}, {"family": "Heidenblad", "given": "Markus", "initials": "M", "orcid": "0000-0002-0668-2263", "researcher": {"href": "https://publications.scilifelab.se/researcher/b49a0816fc794c27a25b34731e8ca7bf.json"}}, {"family": "Leandersson", "given": "Karin", "initials": "K", "orcid": "0000-0001-8254-3137", "researcher": {"href": "https://publications.scilifelab.se/researcher/4736923f382845c2990efb251340bfb4.json"}}, {"family": "Gisselsson", "given": "David", "initials": "D", "orcid": "0000-0002-0301-426X", "researcher": {"href": "https://publications.scilifelab.se/researcher/3653582762b14f9a9ad2fe6aba511115.json"}}, {"family": "Jirstr\u00f6m", "given": "Karin", "initials": "K", "orcid": "0000-0003-2257-5000", "researcher": {"href": "https://publications.scilifelab.se/researcher/9b7c5c8216d943d2b344d9de5622770b.json"}}], "type": "journal article", "published": "2025-10-03", "journal": {"title": "Sci Rep", "issn": "2045-2322", "volume": "15", "issue": "1", "pages": "34481", "issn-l": "2045-2322"}, "abstract": "The vast majority of patients with pancreatic cancer present with unresectable disease and precision medicine is lagging behind. Circulating tumor DNA (ctDNA) has emerged as a promising tool, both as a proxy for tumor burden and for capturing tumor heterogeneity, but optimal gene panels and prognostic cutoffs remain to be determined. Herein, we applied ultra-deep ctDNA sequencing using a customized panel targeting 23 genes and six frequently altered chromosomes on plasma samples obtained before, during and after chemotherapy from 60 patients enrolled in a prospective clinical study. At baseline, positive versus negative ctDNA was not prognostic, neither in the adjuvant nor in the palliative setting, but in palliative patients, an independent prognostic cutoff could be calculated from the absolute number of mutated DNA molecules. Median overall survival was 3.7 months in the ctDNAhigh compared to 11.9 months in the ctDNAlow group (p < 0.0001), and the cutoff remained prognostic at one and three months. Moreover, relevant genetic alterations were highly concordant in ctDNA and paired tumor tissue. These findings demonstrate the potential clinical utility of a customized and focused gene panel for prognostication and target identification over time in patients with newly diagnosed pancreatic cancer, in particular in the palliative setting.ClinicalTrials.gov number: NCT03724994.", "doi": "10.1038/s41598-025-22369-5", "pmid": "41044171", "labels": {"Bioinformatics (NBIS)": "Collaborative", "Bioinformatics Support and Infrastructure": "Collaborative", "Bioinformatics Support, Infrastructure and Training": "Collaborative", "Clinical Genomics Lund": "Service", "Clinical Genomics Stockholm": "Service", "Clinical Genomics": "Service"}, "xrefs": [{"db": "pmc", "key": "PMC12494785"}, {"db": "pii", "key": "10.1038/s41598-025-22369-5"}, {"db": "ClinicalTrials.gov", "key": "NCT03724994"}], "notes": [], "created": "2025-10-16T17:14:10.829Z", "modified": "2025-11-18T20:46:37.775Z"}, {"entity": "publication", "iuid": "11c43093eed24cf3b53703e7743aab32", "links": {"self": {"href": "https://publications.scilifelab.se/publication/11c43093eed24cf3b53703e7743aab32.json"}, "display": {"href": "https://publications.scilifelab.se/publication/11c43093eed24cf3b53703e7743aab32"}}, "title": "The injury-induced transcription factor SOX9 alters the expression of LBR, HMGA2, and HIPK3 in the human kidney.", "authors": [{"family": "Kha", "given": "Michelle", "initials": "M"}, {"family": "Krawczyk", "given": "Krzysztof", "initials": "K"}, {"family": "Choong", "given": "Oi Kuan", "initials": "OK", "orcid": "0000-0003-0257-4748", "researcher": {"href": "https://publications.scilifelab.se/researcher/57045fc513524ab2947dd9f24bac0838.json"}}, {"family": "De Luca", "given": "Francesco", "initials": "F"}, {"family": "Altiparmak", "given": "G\u00fclay", "initials": "G"}, {"family": "K\u00e4llberg", "given": "Eva", "initials": "E"}, {"family": "Nilsson", "given": "Hel\u00e9n", "initials": "H"}, {"family": "Leandersson", "given": "Karin", "initials": "K", "orcid": "0000-0001-8254-3137", "researcher": {"href": "https://publications.scilifelab.se/researcher/4736923f382845c2990efb251340bfb4.json"}}, {"family": "Sw\u00e4rd", "given": "Karl", "initials": "K", "orcid": "0000-0002-7255-5510", "researcher": {"href": "https://publications.scilifelab.se/researcher/b6bf44f11b9d4029bf4bb06ffee09e8c.json"}}, {"family": "Johansson", "given": "Martin E", "initials": "ME", "orcid": "0000-0001-8510-3102", "researcher": {"href": "https://publications.scilifelab.se/researcher/b85588d272854ff2a9d6c4e364529971.json"}}], "type": "journal article", "published": "2023-01-01", "journal": {"title": "Am. J. Physiol. Renal Physiol.", "issn": "1522-1466", "volume": "324", "issue": "1", "pages": "F75-F90", "issn-l": "1522-1466"}, "abstract": "Induction of SRY box transcription factor 9 (SOX9) has been shown to occur in response to kidney injury in rodents, where SOX9-positive cells proliferate and regenerate the proximal tubules of injured kidneys. Additionally, SOX9-positive cells demonstrate a capacity to differentiate toward other nephron segments. Here, we characterized the role of SOX9 in normal and injured human kidneys. SOX9 expression was found to colocalize with a proportion of so-called scattered tubular cells in the uninjured kidney, a cell population previously shown to be involved in kidney injury and regeneration. Following injury and in areas adjacent to inflammatory cell infiltrates, SOX9-positive cells were increased in number. With the use of primary tubular epithelial cells (PTECs) obtained from human kidney tissue, SOX9 expression was spontaneously induced in culture and further increased by transforming growth factor-\u03b21, whereas it was suppressed by interferon-\u03b3. siRNA-mediated knockdown of SOX9 in PTECs followed by analysis of differential gene expression, immunohistochemical expression, and luciferase promoter assays suggested lamin B receptor (LBR), high mobility group AT-hook 2 (HMGA2), and homeodomain interacting protein kinase 3 (HIPK3) as possible target genes of SOX9. Moreover, a kidney explant model was used to demonstrate that only SOX9-positive cells survive the massive injury associated with kidney ischemia and that the surviving SOX9-positive cells spread and repopulate the tubules. Using a wound healing assay, we also showed that SOX9 positively regulated the migratory capacity of PTECs. These findings shed light on the functional and regulatory aspects of SOX9 activation in the human kidney during injury and regeneration.NEW & NOTEWORTHY Recent studies using murine models have shown that SRY box transcription factor 9 (SOX9) is activated during repair of renal tubular cells. In this study, we showed that SOX9-positive cells represent a proportion of scattered tubular cells found in the uninjured human kidney. Furthermore, we suggest that expression of LBR, HMGA2, and HIPK3 is altered by SOX9 in the kidney tubular epithelium, suggesting the involvement of these gene products in kidney injury and regeneration.", "doi": "10.1152/ajprenal.00196.2022", "pmid": "36454702", "labels": {"Clinical Genomics Lund": "Service", "Clinical Genomics Gothenburg": "Service", "Clinical Genomics": "Service"}, "xrefs": [], "notes": [], "created": "2023-02-20T13:56:14.537Z", "modified": "2023-11-30T22:32:49.212Z"}, {"entity": "publication", "iuid": "f3ea7ecc69e24f00b6d9979e061dd885", "links": {"self": {"href": "https://publications.scilifelab.se/publication/f3ea7ecc69e24f00b6d9979e061dd885.json"}, "display": {"href": "https://publications.scilifelab.se/publication/f3ea7ecc69e24f00b6d9979e061dd885"}}, "title": "Human G-MDSCs are neutrophils at distinct maturation stages promoting tumor growth in breast cancer", "authors": [{"family": "Mehmeti-Ajradini", "given": "Meliha", "initials": "M"}, {"family": "Bergenfelz", "given": "Caroline", "initials": "C"}, {"family": "Larsson", "given": "Anna Maria", "initials": "AM"}, {"family": "Carlsson", "given": "Robert", "initials": "R"}, {"family": "Riesbeck", "given": "Kristian", "initials": "K", "orcid": "0000-0001-6274-6965", "researcher": {"href": "https://publications.scilifelab.se/researcher/d757ccad30b043748c8fe48a7308210c.json"}}, {"family": "Ahl", "given": "Jonas", "initials": "J"}, {"family": "Janols", "given": "Helena", "initials": "H"}, {"family": "Wullt", "given": "Marlene", "initials": "M"}, {"family": "Bredberg", "given": "Anders", "initials": "A"}, {"family": "K\u00e4llberg", "given": "Eva", "initials": "E"}, {"family": "Bj\u00f6rk Gunnarsdottir", "given": "Frida", "initials": "F"}, {"family": "Rydberg Millrud", "given": "Camilla", "initials": "C"}, {"family": "Ryd\u00e9n", "given": "Lisa", "initials": "L", "orcid": "0000-0001-7515-3130", "researcher": {"href": "https://publications.scilifelab.se/researcher/424bace557344431a47ffe5cdccbeb56.json"}}, {"family": "Paul", "given": "Gesine", "initials": "G"}, {"family": "Loman", "given": "Niklas", "initials": "N"}, {"family": "Adolfsson", "given": "J\u00f6rgen", "initials": "J"}, {"family": "Carneiro", "given": "Ana", "initials": "A", "orcid": "0000-0002-1818-7008", "researcher": {"href": "https://publications.scilifelab.se/researcher/12ef95bff08743398bf3a374195e043e.json"}}, {"family": "Jirstr\u00f6m", "given": "Karin", "initials": "K"}, {"family": "Killander", "given": "Fredrika", "initials": "F"}, {"family": "Bexell", "given": "Daniel", "initials": "D"}, {"family": "Leandersson", "given": "Karin", "initials": "K", "orcid": "0000-0001-8254-3137", "researcher": {"href": "https://publications.scilifelab.se/researcher/4736923f382845c2990efb251340bfb4.json"}}], "type": "journal-article", "published": "2020-11-00", "journal": {"title": "Life Sci. Alliance", "issn": "2575-1077", "issn-l": "2575-1077", "volume": "3", "issue": "11", "pages": "e202000893"}, "abstract": "Myeloid-derived suppressor cells (MDSCs) are known to contribute to immune evasion in cancer. However, the function of the human granulocytic (G)-MDSC subset during tumor progression is largely unknown, and there are no established markers for their identification in human tumor specimens. Using gene expression profiling, mass cytometry, and tumor microarrays, we here demonstrate that human G-MDSCs occur as neutrophils at distinct maturation stages, with a disease-specific profile. G-MDSCs derived from patients with metastatic breast cancer and malignant melanoma display a unique immature neutrophil profile, that is more similar to healthy donor neutrophils than to G-MDSCs from sepsis patients. Finally, we show that primary G-MDSCs from metastatic breast cancer patients co-transplanted with breast cancer cells, promote tumor growth, and affect vessel formation, leading to myeloid immune cell exclusion. Our findings reveal a role for human G-MDSC in tumor progression and have clinical implications also for targeted immunotherapy.", "doi": "10.26508/lsa.202000893", "pmid": "32958605", "labels": {"Cellular Immunomonitoring": "Service", "Bioinformatics Support, Infrastructure and Training": "Service", "Bioinformatics Support and Infrastructure": "Service", "Bioinformatics (NBIS)": "Service"}, "xrefs": [{"db": "pmc", "key": "PMC7536824"}, {"db": "pii", "key": "3/11/e202000893"}], "notes": [], "created": "2020-09-24T15:35:44.836Z", "modified": "2024-11-15T09:54:18.581Z"}, {"entity": "publication", "iuid": "42facd6bed944bae835b71cba9824a4f", "links": {"self": {"href": "https://publications.scilifelab.se/publication/42facd6bed944bae835b71cba9824a4f.json"}, "display": {"href": "https://publications.scilifelab.se/publication/42facd6bed944bae835b71cba9824a4f"}}, "title": "Wnt5a is a TLR2/4-ligand that induces tolerance in human myeloid cells.", "authors": [{"family": "Mehmeti", "given": "Meliha", "initials": "M"}, {"family": "Bergenfelz", "given": "Caroline", "initials": "C"}, {"family": "K\u00e4llberg", "given": "Eva", "initials": "E"}, {"family": "Millrud", "given": "Camilla Rydberg", "initials": "CR"}, {"family": "Bj\u00f6rk", "given": "Per", "initials": "P"}, {"family": "Ivars", "given": "Fredrik", "initials": "F"}, {"family": "Johansson-Lindbom", "given": "Bengt", "initials": "B"}, {"family": "Kjellstr\u00f6m", "given": "Sven", "initials": "S"}, {"family": "Andr\u00e9", "given": "Ingemar", "initials": "I"}, {"family": "Leandersson", "given": "Karin", "initials": "K", "orcid": "0000-0001-8254-3137", "researcher": {"href": "https://publications.scilifelab.se/researcher/4736923f382845c2990efb251340bfb4.json"}}], "type": "journal article", "published": "2019-05-09", "journal": {"title": "Commun Biol", "issn": "2399-3642", "volume": "2", "issue": "1", "pages": "176", "issn-l": "2399-3642"}, "abstract": "Innate immune responses are rapid, dynamic and highly regulated to avoid overt reactions. This regulation is executed by innate immune tolerance mechanisms that remain obscure. Wnt5a is a signalling protein mainly involved in developmental processes and cancer. The effect of Wnt5a on inflammatory myeloid cells is controversial. Here, we combine primary cell cultures, in vitro binding studies, mass spectrometry and Drosophila protein modelling to show that Wnt5a is a direct ligand of toll-like receptor (TLR) 2 and 4. The binding promotes a MyD88-non-canonical nuclear factor of kappa B (NF\u03baB) and AP-1 signalling cascade, with contradictory profiles in mouse (pro-inflammatory) and human (anti-inflammatory) myeloid immune cells. These data reveal that the true nature of Wnt5a in inflammatory cells, is to regulate TLR signals, and in human myeloid cells it acts as an endogenous, tolerance-associated molecular pattern (TAMP), inducing IL-10 and innate immune tolerance.", "doi": "10.1038/s42003-019-0432-4", "pmid": "31098409", "labels": {"Structural Proteomics": "Service"}, "xrefs": [{"db": "pii", "key": "432"}, {"db": "pmc", "key": "PMC6509336"}], "notes": [], "created": "2020-01-27T10:00:20.654Z", "modified": "2021-06-16T14:55:04.785Z"}]}