{"entity": "researcher", "timestamp": "2026-09-24T16:25:54.146Z", "family": "Stratmann", "given": "Svea", "initials": "S", "orcid": "0000-0002-7438-9093", "affiliations": ["Department of Immunology, Genetics and Pathology, Science for Life Laboratory, Uppsala University, Uppsala, Sweden."], "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/researcher/65a4f696205a4d6e8bddc3d0060d98a3.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/researcher/65a4f696205a4d6e8bddc3d0060d98a3"}}, "publications": [{"entity": "publication", "iuid": "0738a68adbde4dd08427fb547b8697e0", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/0738a68adbde4dd08427fb547b8697e0.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/0738a68adbde4dd08427fb547b8697e0"}}, "title": "Proteogenomic analysis of acute myeloid leukemia associates relapsed disease with reprogrammed energy metabolism both in adults and children.", "authors": [{"family": "Stratmann", "given": "Svea", "initials": "S", "orcid": "0000-0002-7438-9093", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/65a4f696205a4d6e8bddc3d0060d98a3.json"}}, {"family": "Vesterlund", "given": "Mattias", "initials": "M", "orcid": "0000-0001-9471-6592", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/e443cdb01cc44a7fa786941b5c0b62d6.json"}}, {"family": "Umer", "given": "Husen M", "initials": "HM", "orcid": "0000-0003-3971-2462", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/922625c410444833a263244d0313980e.json"}}, {"family": "Eshtad", "given": "Saeed", "initials": "S"}, {"family": "Skaftason", "given": "Aron", "initials": "A"}, {"family": "Herlin", "given": "Morten Krogh", "initials": "MK", "orcid": "0000-0001-7179-4643", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/0d267c8019a941919afcad35c891fa55.json"}}, {"family": "Sundstr\u00f6m", "given": "Christer", "initials": "C", "orcid": "0000-0002-8160-5647", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/362f4bd03caa4154bd5c9ed8c9c7213a.json"}}, {"family": "Eriksson", "given": "Anna", "initials": "A", "orcid": "0000-0002-8853-1863", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/d37bf77253344a92968b4adb46c6f98c.json"}}, {"family": "H\u00f6glund", "given": "Martin", "initials": "M"}, {"family": "Palle", "given": "Josefine", "initials": "J"}, {"family": "Abrahamsson", "given": "Jonas", "initials": "J"}, {"family": "Jahnukainen", "given": "Kirsi", "initials": "K", "orcid": "0000-0001-9296-2028", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/532aaf3e2e8847d5867bd7e30dd75137.json"}}, {"family": "Munthe-Kaas", "given": "Monica Cheng", "initials": "MC"}, {"family": "Zeller", "given": "Bernward", "initials": "B"}, {"family": "Tamm", "given": "Katja Pokrovskaja", "initials": "KP", "orcid": "0000-0001-6359-1256", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/063e26c562c74bc2a4eab139d7818f2c.json"}}, {"family": "Lindskog", "given": "Cecilia", "initials": "C"}, {"family": "Cavelier", "given": "Lucia", "initials": "L"}, {"family": "Lehti\u00f6", "given": "Janne", "initials": "J", "orcid": "0000-0002-8100-9562", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/561efcf32e2648c8a10fee692fc4e908.json"}}, {"family": "Holmfeldt", "given": "Linda", "initials": "L", "orcid": "0000-0003-4140-3423", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/13a857b0c5b64d10a8e3b6b70d4dc662.json"}}], "type": "journal article", "published": "2023-03-00", "journal": {"title": "Leukemia", "issn": "1476-5551", "volume": "37", "issue": "3", "pages": "550-559", "issn-l": "0887-6924"}, "abstract": "Despite improvement of current treatment strategies and novel targeted drugs, relapse and treatment resistance largely determine the outcome for acute myeloid leukemia (AML) patients. To identify the underlying molecular characteristics, numerous studies have been aimed to decipher the genomic- and transcriptomic landscape of AML. Nevertheless, further molecular changes allowing malignant cells to escape treatment remain to be elucidated. Mass spectrometry is a powerful tool enabling detailed insights into proteomic changes that could explain AML relapse and resistance. Here, we investigated AML samples from 47 adult and 22 pediatric patients at serial time-points during disease progression using mass spectrometry-based in-depth proteomics. We show that the proteomic profile at relapse is enriched for mitochondrial ribosomal proteins and subunits of the respiratory chain complex, indicative of reprogrammed energy metabolism from diagnosis to relapse. Further, higher levels of granzymes and lower levels of the anti-inflammatory protein CR1/CD35 suggest an inflammatory signature promoting disease progression. Finally, through a proteogenomic approach, we detected novel peptides, which present a promising repertoire in the search for biomarkers and tumor-specific druggable targets. Altogether, this study highlights the importance of proteomic studies in holistic approaches to improve treatment and survival of AML patients.", "doi": "10.1038/s41375-022-01796-7", "pmid": "36572751", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC9991901"}, {"db": "pii", "key": "10.1038/s41375-022-01796-7"}], "notes": [], "created": "2026-09-23T08:51:06.323Z", "modified": "2026-09-23T08:51:06.601Z"}, {"entity": "publication", "iuid": "20afff445ad84ccc9b31e5c8c1ed7b28", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/20afff445ad84ccc9b31e5c8c1ed7b28.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/20afff445ad84ccc9b31e5c8c1ed7b28"}}, "title": "Transcriptomic analysis reveals proinflammatory signatures associated with acute myeloid leukemia progression.", "authors": [{"family": "Stratmann", "given": "Svea", "initials": "S", "orcid": "0000-0002-7438-9093", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/65a4f696205a4d6e8bddc3d0060d98a3.json"}}, {"family": "Yones", "given": "Sara A", "initials": "SA", "orcid": "0000-0002-7201-2604", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/a1db6ae5db964f149ffc93ea78561711.json"}}, {"family": "Garbulowski", "given": "Mateusz", "initials": "M", "orcid": "0000-0002-2497-194X", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/98de355d5a1247cebb494b16444857e6.json"}}, {"family": "Sun", "given": "Jitong", "initials": "J"}, {"family": "Skaftason", "given": "Aron", "initials": "A"}, {"family": "Mayrhofer", "given": "Markus", "initials": "M"}, {"family": "Norgren", "given": "Nina", "initials": "N", "orcid": "0000-0002-3823-1555", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/e771ac8f26354dcc980b67b51594b687.json"}}, {"family": "Herlin", "given": "Morten Krogh", "initials": "MK", "orcid": "0000-0001-7179-4643", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/0d267c8019a941919afcad35c891fa55.json"}}, {"family": "Sundstr\u00f6m", "given": "Christer", "initials": "C", "orcid": "0000-0002-8160-5647", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/362f4bd03caa4154bd5c9ed8c9c7213a.json"}}, {"family": "Eriksson", "given": "Anna", "initials": "A"}, {"family": "H\u00f6glund", "given": "Martin", "initials": "M", "orcid": "0000-0003-2468-0226", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/b04dde8160944595a255121a2571d2da.json"}}, {"family": "Palle", "given": "Josefine", "initials": "J"}, {"family": "Abrahamsson", "given": "Jonas", "initials": "J"}, {"family": "Jahnukainen", "given": "Kirsi", "initials": "K"}, {"family": "Munthe-Kaas", "given": "Monica Cheng", "initials": "MC"}, {"family": "Zeller", "given": "Bernward", "initials": "B"}, {"family": "Tamm", "given": "Katja Pokrovskaja", "initials": "KP"}, {"family": "Cavelier", "given": "Lucia", "initials": "L"}, {"family": "Komorowski", "given": "Jan", "initials": "J", "orcid": "0000-0002-0766-8789", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/1dffb9dd373741069230b4f80d7e1698.json"}}, {"family": "Holmfeldt", "given": "Linda", "initials": "L", "orcid": "0000-0003-4140-3423", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/13a857b0c5b64d10a8e3b6b70d4dc662.json"}}], "type": "journal article", "published": "2022-01-11", "journal": {"title": "Blood Adv", "issn": "2473-9529", "volume": "6", "issue": "1", "pages": "152-164", "issn-l": null}, "abstract": "Numerous studies have been performed over the last decade to exploit the complexity of genomic and transcriptomic lesions driving the initiation of acute myeloid leukemia (AML). These studies have helped improve risk classification and treatment options. Detailed molecular characterization of longitudinal AML samples is sparse, however; meanwhile, relapse and therapy resistance represent the main challenges in AML care. To this end, we performed transcriptome-wide RNA sequencing of longitudinal diagnosis, relapse, and/or primary resistant samples from 47 adult and 23 pediatric AML patients with known mutational background. Gene expression analysis revealed the association of short event-free survival with overexpression of GLI2 and IL1R1, as well as downregulation of ST18. Moreover, CR1 downregulation and DPEP1 upregulation were associated with AML relapse both in adults and children. Finally, machine learning-based and network-based analysis identified overexpressed CD6 and downregulated INSR as highly copredictive genes depicting important relapse-associated characteristics among adult patients with AML. Our findings highlight the importance of a tumor-promoting inflammatory environment in leukemia progression, as indicated by several of the herein identified differentially expressed genes. Together, this knowledge provides the foundation for novel personalized drug targets and has the potential to maximize the benefit of current treatments to improve cure rates in AML.", "doi": "10.1182/bloodadvances.2021004962", "pmid": "34619772", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC8753201"}, {"db": "pii", "key": "477210"}], "notes": [], "created": "2026-09-23T08:52:58.969Z", "modified": "2026-09-23T08:52:59.063Z"}]}