{"entity": "researcher", "timestamp": "2026-08-15T06:55:54.271Z", "family": "Landberg", "given": "Niklas", "initials": "N", "orcid": "0000-0001-6752-6507", "affiliations": ["Division of Clinical Genetics, Department of Laboratory Medicine, Lund University, Lund, Sweden.", "Department of Hematology, Oncology and Radiation Physics, Sk\u00e5ne University Hospital, Lund, Sweden."], "links": {"self": {"href": "https://publications.scilifelab.se/researcher/1ad422be3ea44e419662d514ca40cbbe.json"}, "display": {"href": "https://publications.scilifelab.se/researcher/1ad422be3ea44e419662d514ca40cbbe"}}, "publications": [{"entity": "publication", "iuid": "c2874ad4279747de98010159c6b2bbcc", "links": {"self": {"href": "https://publications.scilifelab.se/publication/c2874ad4279747de98010159c6b2bbcc.json"}, "display": {"href": "https://publications.scilifelab.se/publication/c2874ad4279747de98010159c6b2bbcc"}}, "title": "Aberrant expression of SLAMF6 constitutes a targetable immune escape mechanism in acute myeloid leukemia.", "authors": [{"family": "Sand\u00e9n", "given": "Carl", "initials": "C", "orcid": "0000-0002-8931-9565", "researcher": {"href": "https://publications.scilifelab.se/researcher/29207805704e4660b20eebc87efe5282.json"}}, {"family": "Landberg", "given": "Niklas", "initials": "N", "orcid": "0000-0001-6752-6507", "researcher": {"href": "https://publications.scilifelab.se/researcher/1ad422be3ea44e419662d514ca40cbbe.json"}}, {"family": "Pe\u00f1a-Mart\u00ednez", "given": "Pablo", "initials": "P", "orcid": "0000-0002-0789-6431", "researcher": {"href": "https://publications.scilifelab.se/researcher/6d675e892dfc4334bb12051e004a7711.json"}}, {"family": "Thorsson", "given": "Hanna", "initials": "H", "orcid": "0000-0001-5393-2942", "researcher": {"href": "https://publications.scilifelab.se/researcher/7667559679a64a999d508ff7fa506782.json"}}, {"family": "Daga", "given": "Shruti", "initials": "S"}, {"family": "Puente-Moncada", "given": "Noelia", "initials": "N"}, {"family": "Rodriguez-Zabala", "given": "Maria", "initials": "M"}, {"family": "von Palffy", "given": "Sofia", "initials": "S"}, {"family": "Rissler", "given": "Marianne", "initials": "M"}, {"family": "Lazarevic", "given": "Vladimir", "initials": "V", "orcid": "0000-0002-1782-4423", "researcher": {"href": "https://publications.scilifelab.se/researcher/7113f0d0569247d4ac94b73ddc6ca74e.json"}}, {"family": "Juliusson", "given": "Gunnar", "initials": "G"}, {"family": "Ohlin", "given": "Mats", "initials": "M", "orcid": "0000-0002-5105-1938", "researcher": {"href": "https://publications.scilifelab.se/researcher/fda1d1ed0b074a04a69b0c8b036dd001.json"}}, {"family": "Hyrenius-Wittsten", "given": "Axel", "initials": "A"}, {"family": "Orsmark-Pietras", "given": "Christina", "initials": "C", "orcid": "0000-0002-6533-0305", "researcher": {"href": "https://publications.scilifelab.se/researcher/66a38c96c9854fb18eb2420689d620e2.json"}}, {"family": "Lilljebj\u00f6rn", "given": "Henrik", "initials": "H", "orcid": "0000-0001-8703-1173", "researcher": {"href": "https://publications.scilifelab.se/researcher/b3a75300e8c346858ce8dd8f64ecae85.json"}}, {"family": "\u00c5gerstam", "given": "Helena", "initials": "H"}, {"family": "Fioretos", "given": "Thoas", "initials": "T", "orcid": "0000-0002-3235-6154", "researcher": {"href": "https://publications.scilifelab.se/researcher/35a5c1b6023345c6b1317c590bf80680.json"}}], "type": "journal article", "published": "2025-11-00", "journal": {"title": "Nat Cancer", "issn": "2662-1347", "volume": "6", "issue": "11", "pages": "1821-1838", "issn-l": null}, "abstract": "Immunotherapy has shown limited success in acute myeloid leukemia (AML), indicating an incomplete understanding of the underlying immunoregulatory mechanisms. Here we identify an immune evasion mechanism present in 60% of AML cases, wherein primitive AML cells aberrantly express the lymphoid surface protein SLAMF6 (signaling lymphocyte activation molecule family member 6). Knockout of SLAMF6 in AML cells enables T cell activation and highly efficient killing of leukemia cells in coculture systems, demonstrating that SLAMF6 protects AML cells from recognition and elimination by the immune system in a mode analogous to the programmed cell death protein-ligand (PDL1/PD1) axis. Targeting SLAMF6 with an antibody against the SLAMF6 dimerization site inhibits the SLAMF6-SLAMF6 interaction and induces T cell activation and killing of AML cells both in vitro and in humanized in vivo models. In conclusion, we show that aberrant expression of SLAMF6 is a common and targetable immune escape mechanism that could pave the way for immunotherapy in AML.", "doi": "10.1038/s43018-025-01054-6", "pmid": "41044242", "labels": {"Clinical Genomics Lund": "Service", "Drug Discovery and Development": "Collaborative", "Structural Proteomics": "Service"}, "xrefs": [{"db": "pii", "key": "10.1038/s43018-025-01054-6"}, {"db": "pmc", "key": "PMC12643940"}], "notes": [], "created": "2025-11-05T18:37:31.700Z", "modified": "2025-11-26T16:29:09.833Z"}, {"entity": "publication", "iuid": "c91e733931184d15a4991de3419a6d4d", "links": {"self": {"href": "https://publications.scilifelab.se/publication/c91e733931184d15a4991de3419a6d4d.json"}, "display": {"href": "https://publications.scilifelab.se/publication/c91e733931184d15a4991de3419a6d4d"}}, "title": "The complement receptor C3AR constitutes a novel therapeutic target in NPM1-mutated AML.", "authors": [{"family": "von Palffy", "given": "Sofia", "initials": "S", "orcid": "0000-0001-5640-4037", "researcher": {"href": "https://publications.scilifelab.se/researcher/594eb39f228241efb0f055799f5eaa88.json"}}, {"family": "Thorsson", "given": "Hanna", "initials": "H"}, {"family": "Pe\u00f1a-Mart\u00ednez", "given": "Pablo", "initials": "P", "orcid": "0000-0002-0789-6431", "researcher": {"href": "https://publications.scilifelab.se/researcher/6d675e892dfc4334bb12051e004a7711.json"}}, {"family": "Puente-Moncada", "given": "Noelia", "initials": "N", "orcid": "0000-0002-5996-2349", "researcher": {"href": "https://publications.scilifelab.se/researcher/1d4ac0bd551b4463a22e3f60470c2b6d.json"}}, {"family": "Sand\u00e9n", "given": "Carl", "initials": "C", "orcid": "0000-0002-8931-9565", "researcher": {"href": "https://publications.scilifelab.se/researcher/29207805704e4660b20eebc87efe5282.json"}}, {"family": "Blom", "given": "Anna M", "initials": "AM", "orcid": "0000-0002-1348-1734", "researcher": {"href": "https://publications.scilifelab.se/researcher/c18466d1f5614ecbb63c5d4136a02466.json"}}, {"family": "Henningsson", "given": "Rasmus", "initials": "R"}, {"family": "Juliusson", "given": "Gunnar", "initials": "G"}, {"family": "King", "given": "Ben", "initials": "B", "orcid": "0000-0001-6776-8741", "researcher": {"href": "https://publications.scilifelab.se/researcher/108b9f873836471697d74d10dd9f8707.json"}}, {"family": "Landberg", "given": "Niklas", "initials": "N", "orcid": "0000-0001-6752-6507", "researcher": {"href": "https://publications.scilifelab.se/researcher/1ad422be3ea44e419662d514ca40cbbe.json"}}, {"family": "Lazarevic", "given": "Vladimir", "initials": "V", "orcid": "0000-0002-1782-4423", "researcher": {"href": "https://publications.scilifelab.se/researcher/7113f0d0569247d4ac94b73ddc6ca74e.json"}}, {"family": "Orsmark-Pietras", "given": "Christina", "initials": "C"}, {"family": "Rissler", "given": "Marianne", "initials": "M"}, {"family": "Rissler", "given": "Vendela", "initials": "V"}, {"family": "\u00c5gerstam", "given": "Helena", "initials": "H"}, {"family": "J\u00e4r\u00e5s", "given": "Marcus", "initials": "M"}, {"family": "Lilljebj\u00f6rn", "given": "Henrik", "initials": "H"}, {"family": "Fioretos", "given": "Thoas", "initials": "T"}], "type": "journal article", "published": "2023-04-11", "journal": {"title": "Blood Adv", "issn": "2473-9537", "volume": "7", "issue": "7", "pages": "1204-1218", "issn-l": "2473-9529"}, "abstract": "Mutated nucleophosmin 1 (NPM1) is the most common genetic alteration in acute myeloid leukemia (AML), found in \u223c30% of cases. Although mutations in this gene are considered favorable according to current risk stratification guidelines, a large fraction of patients will experience relapse, demonstrating the urgent need for new treatment options. Therefore, we aimed to identify cell surface proteins specifically expressed on NPM1-mutated AML cells, allowing for potential targeting with antibody-based therapies. Herein, we report on an arrayed flow cytometry-based screen directed to 362 cell surface markers. In comparing the cell surface expression on NPM1-mutated AML cells with primitive (CD34+ CD38-) normal bone marrow cells, we identified the complement receptor C3AR as being specifically expressed in NPM1-mutated AML. By flow cytometry and single-cell RNA sequencing, we further show that normal hematopoietic stem and progenitor cells lack detectable C3AR gene and protein expression, making it particularly suitable as a target for antibody therapy. We also demonstrate that C3AR in combination with GPR56 distinguishes the leukemic stem cells (LSCs) in NPM1-mutated AML from the normal hematopoietic stem cells, defining the LSC population, as shown by transplantation into immunodeficient mice. Mechanistically, the stimulation of C3AR-expressing cells with C3a, the ligand of C3AR, leads to the activation of ERK1/2 and increased survival of AML cells, suggesting that this is an important signaling axis in this subtype of AML. Finally, we show that antibodies directed against C3AR efficiently elicit natural killer cell-mediated killing of primary AML cells ex vivo, highlighting C3AR as a candidate therapeutic target in NPM1-mutated AML.", "doi": "10.1182/bloodadvances.2022007682", "pmid": "36383712", "labels": {"Clinical Genomics Lund": "Service", "Clinical Genomics": "Service"}, "xrefs": [{"db": "pmc", "key": "PMC10111354"}, {"db": "pii", "key": "493242"}], "notes": [], "created": "2023-02-20T13:51:41.288Z", "modified": "2024-01-07T18:37:55.987Z"}, {"entity": "publication", "iuid": "7e69f131beb747948a82b285b2993442", "links": {"self": {"href": "https://publications.scilifelab.se/publication/7e69f131beb747948a82b285b2993442.json"}, "display": {"href": "https://publications.scilifelab.se/publication/7e69f131beb747948a82b285b2993442"}}, "title": "Clonal competition within complex evolutionary hierarchies shapes AML over time.", "authors": [{"family": "Sand\u00e9n", "given": "Carl", "initials": "C", "orcid": "0000-0002-8931-9565", "researcher": {"href": "https://publications.scilifelab.se/researcher/29207805704e4660b20eebc87efe5282.json"}}, {"family": "Lilljebj\u00f6rn", "given": "Henrik", "initials": "H", "orcid": "0000-0001-8703-1173", "researcher": {"href": "https://publications.scilifelab.se/researcher/b3a75300e8c346858ce8dd8f64ecae85.json"}}, {"family": "Orsmark Pietras", "given": "Christina", "initials": "C"}, {"family": "Henningsson", "given": "Rasmus", "initials": "R"}, {"family": "Saba", "given": "Karim H", "initials": "KH", "orcid": "0000-0003-4946-6488", "researcher": {"href": "https://publications.scilifelab.se/researcher/42cc0dd26f394abb9117550f4e5a034c.json"}}, {"family": "Landberg", "given": "Niklas", "initials": "N", "orcid": "0000-0001-6752-6507", "researcher": {"href": "https://publications.scilifelab.se/researcher/1ad422be3ea44e419662d514ca40cbbe.json"}}, {"family": "Thorsson", "given": "Hanna", "initials": "H"}, {"family": "von Palffy", "given": "Sofia", "initials": "S", "orcid": "0000-0001-5640-4037", "researcher": {"href": "https://publications.scilifelab.se/researcher/594eb39f228241efb0f055799f5eaa88.json"}}, {"family": "Pe\u00f1a-Martinez", "given": "Pablo", "initials": "P", "orcid": "0000-0002-0789-6431", "researcher": {"href": "https://publications.scilifelab.se/researcher/6d675e892dfc4334bb12051e004a7711.json"}}, {"family": "H\u00f6gberg", "given": "Carl", "initials": "C"}, {"family": "Rissler", "given": "Marianne", "initials": "M"}, {"family": "Gisselsson", "given": "David", "initials": "D", "orcid": "0000-0002-0301-426X", "researcher": {"href": "https://publications.scilifelab.se/researcher/3653582762b14f9a9ad2fe6aba511115.json"}}, {"family": "Lazarevic", "given": "Vladimir", "initials": "V", "orcid": "0000-0002-1782-4423", "researcher": {"href": "https://publications.scilifelab.se/researcher/7113f0d0569247d4ac94b73ddc6ca74e.json"}}, {"family": "Juliusson", "given": "Gunnar", "initials": "G"}, {"family": "\u00c5gerstam", "given": "Helena", "initials": "H"}, {"family": "Fioretos", "given": "Thoas", "initials": "T", "orcid": "0000-0002-3235-6154", "researcher": {"href": "https://publications.scilifelab.se/researcher/35a5c1b6023345c6b1317c590bf80680.json"}}], "type": "journal article", "published": "2020-02-05", "journal": {"title": "Nat Commun", "issn": "2041-1723", "volume": "11", "issue": "1", "pages": "579", "issn-l": "2041-1723"}, "abstract": "Clonal heterogeneity and evolution has major implications for disease progression and relapse in acute myeloid leukemia (AML). To model clonal dynamics in vivo, we serially transplanted 23 AML cases to immunodeficient mice and followed clonal composition for up to 15 months by whole-exome sequencing of 84 xenografts across two generations. We demonstrate vast changes in clonality that both progress and reverse over time, and define five patterns of clonal dynamics: Monoclonal, Stable, Loss, Expansion and Burst. We also show that subclonal expansion in vivo correlates with a more adverse prognosis. Furthermore, clonal expansion enabled detection of very rare clones with AML driver mutations that were undetectable by sequencing at diagnosis, demonstrating that the vast majority of AML cases harbor multiple clones already at diagnosis. Finally, the rise and fall of related clones enabled deconstruction of the complex evolutionary hierarchies of the clones that compete to shape AML over time.", "doi": "10.1038/s41467-019-14106-0", "pmid": "32024830", "labels": {"Clinical Genomics Lund": null, "Clinical Genomics": null}, "xrefs": [{"db": "pii", "key": "10.1038/s41467-019-14106-0"}, {"db": "pmc", "key": "PMC7002407"}], "notes": [], "created": "2020-02-24T10:54:40.951Z", "modified": "2021-11-10T12:54:09.856Z"}]}