{"entity": "researcher", "timestamp": "2026-10-11T05:13:38.274Z", "family": "Zhong", "given": "Xiangfu", "initials": "X", "orcid": "0000-0002-1872-1186", "affiliations": ["Department of Medicine, Center for Hematology and Regenerative Medicine, Karolinska Institute, Huddinge, Sweden.", "Department of Medical Sciences, Hematology, Uppsala University, Uppsala, Sweden."], "links": {"self": {"href": "https://publications.scilifelab.se/researcher/b625a888935a42a89d7df3522e249413.json"}, "display": {"href": "https://publications.scilifelab.se/researcher/b625a888935a42a89d7df3522e249413"}}, "publications": [{"entity": "publication", "iuid": "62e45af9d03f4521ad79360efb4f3d00", "links": {"self": {"href": "https://publications.scilifelab.se/publication/62e45af9d03f4521ad79360efb4f3d00.json"}, "display": {"href": "https://publications.scilifelab.se/publication/62e45af9d03f4521ad79360efb4f3d00"}}, "title": "Identification of long non-coding RNAs involved in leukemogenesis and venetoclax response in acute myeloid leukemia through functional CRISPR-dCas9 interference screens.", "authors": [{"family": "Cozzi", "given": "Elisabetta", "initials": "E", "orcid": "0009-0003-5311-7974", "researcher": {"href": "https://publications.scilifelab.se/researcher/bb6657fdce5a4c8e99ad05f000ef8de3.json"}}, {"family": "Neddermeyer", "given": "Anne", "initials": "A"}, {"family": "Miliara", "given": "Sophia", "initials": "S"}, {"family": "Zhong", "given": "Xiangfu", "initials": "X", "orcid": "0000-0002-1872-1186", "researcher": {"href": "https://publications.scilifelab.se/researcher/b625a888935a42a89d7df3522e249413.json"}}, {"family": "Weirick", "given": "Tyler", "initials": "T", "orcid": "0000-0003-0110-5712", "researcher": {"href": "https://publications.scilifelab.se/researcher/0357a7a244b44367a7e3a60e4accb076.json"}}, {"family": "Struyf", "given": "Nona", "initials": "N", "orcid": "0000-0002-6975-0753", "researcher": {"href": "https://publications.scilifelab.se/researcher/1295c3be31024c4fa2da10cffe42c406.json"}}, {"family": "Erkers", "given": "Tom", "initials": "T"}, {"family": "Hon", "given": "Chung Chau", "initials": "CC"}, {"family": "Lennartsson", "given": "Andreas", "initials": "A"}, {"family": "Lehmann", "given": "S\u00f6ren", "initials": "S", "orcid": "0000-0001-8374-8978", "researcher": {"href": "https://publications.scilifelab.se/researcher/4be462a447404937857936f77677da2f.json"}}], "type": "journal article", "published": "2026-10-00", "journal": {"title": "Noncoding RNA Res", "issn": "2468-0540", "issn-l": null, "volume": "20", "issue": null, "pages": "29-43"}, "abstract": "Acute myeloid leukemia (AML) is a malignant hematologic disease with poor prognosis, and improved understanding of its biology is critical for patient outcomes. While protein-coding genes in AML are well characterized, the role of long non-coding RNAs (lncRNAs) remains largely unexplored. Here, we investigated how lncRNAs contribute to AML biology and treatment resistance. Three high-throughput lncRNA-CRISPR-interference (CRISPRi) screens were performed in the AML cell line MOLM-13, targeting 7996 lncRNAs expressed in hematopoietic cells, with knockdowns directed to transcription start sites defined through cap analysis of gene expression (CAGE) sequencing. Effects on proliferation, differentiation, and response to the Bcl-2 inhibitor venetoclax were assessed. In total, 58, 4, and 23 lncRNAs were found to affect proliferation, differentiation, and venetoclax sensitivity, respectively. Three proliferation-associated lncRNAs (MIR17HG, CATG00000106133.1, and CATG00000056792.1) and one venetoclax-associated lncRNA (AC009299.3) were further investigated. CATG00000106133.1 was enriched in de novo and cytogenetically normal AML and correlated with NPM1 and IDH2 mutations. Gene Ontology and Reactome analyses of RNA-seq from CATG00000106133.1 knockout cells revealed roles in cytokine signaling and immune pathways. AC009299.3, linked to venetoclax response, was associated with poor outcome, adverse risk, and increased age in AML patients. Collectively, this study identifies four lncRNAs implicated in key leukemogenic processes, highlighting their potential for understanding AML biology, prognosis, and therapeutic response.", "doi": "10.1016/j.ncrna.2026.05.002", "pmid": "42388349", "labels": {"CRISPR Functional Genomics": "Service", "NGI Short read": "Service", "NGI Stockholm (Genomics Production)": "Service", "National Genomics Infrastructure": "Service"}, "xrefs": [{"db": "pmc", "key": "PMC13318546"}, {"db": "pii", "key": "S2468-0540(26)00043-0"}], "notes": [], "created": "2026-09-13T11:29:14.660Z", "modified": "2026-10-07T09:46:56.192Z"}, {"entity": "publication", "iuid": "4ed7da9adac244919a18efaef8b67a03", "links": {"self": {"href": "https://publications.scilifelab.se/publication/4ed7da9adac244919a18efaef8b67a03.json"}, "display": {"href": "https://publications.scilifelab.se/publication/4ed7da9adac244919a18efaef8b67a03"}}, "title": "MALNC: a new mutant NPM1/IDH2R140 and PML-RARA-associated lncRNA with impact on AML cell proliferation, maturation and drug response.", "authors": [{"family": "Cozzi", "given": "Elisabetta", "initials": "E", "orcid": "0009-0003-5311-7974", "researcher": {"href": "https://publications.scilifelab.se/researcher/bb6657fdce5a4c8e99ad05f000ef8de3.json"}}, {"family": "Neddermeyer", "given": "Anne", "initials": "A"}, {"family": "Zhong", "given": "Xiangfu", "initials": "X", "orcid": "0000-0002-1872-1186", "researcher": {"href": "https://publications.scilifelab.se/researcher/b625a888935a42a89d7df3522e249413.json"}}, {"family": "Gamboa-Cede\u00f1o", "given": "Angelica Mar\u00eda", "initials": "AM"}, {"family": "Kanellis", "given": "Dimitris C", "initials": "DC", "orcid": "0000-0001-8690-2010", "researcher": {"href": "https://publications.scilifelab.se/researcher/0921ab7566514fb0a3cd0daf2baabe6e.json"}}, {"family": "\u00d6sterroos", "given": "Albin", "initials": "A"}, {"family": "Bj\u00f6rklund", "given": "My", "initials": "M", "orcid": "0000-0002-2325-6012", "researcher": {"href": "https://publications.scilifelab.se/researcher/3cc743cdb2604ffdbc78303d70985c48.json"}}, {"family": "Struyf", "given": "Nona", "initials": "N"}, {"family": "Karlsson", "given": "Kasper", "initials": "K"}, {"family": "Qu", "given": "Ying", "initials": "Y"}, {"family": "M\u00e5nsson", "given": "Alma", "initials": "A", "orcid": "0009-0006-1982-7712", "researcher": {"href": "https://publications.scilifelab.se/researcher/6ccda3e6f49f43f5bcf5576d7acc16e5.json"}}, {"family": "Pandzic", "given": "Tatjana", "initials": "T"}, {"family": "Bengtz\u00e9n", "given": "Sofia", "initials": "S"}, {"family": "Nilsson", "given": "Christer", "initials": "C", "orcid": "0000-0003-0695-0050", "researcher": {"href": "https://publications.scilifelab.se/researcher/7f78180b33fa48cd86474d5c3cdaa852.json"}}, {"family": "Fiskesund", "given": "Roland", "initials": "R"}, {"family": "Baliakas", "given": "Panagiotis", "initials": "P", "orcid": "0000-0002-5634-7156", "researcher": {"href": "https://publications.scilifelab.se/researcher/17370bd509dc4b1081af5aed9e5117c7.json"}}, {"family": "Erkers", "given": "Tom", "initials": "T"}, {"family": "Bartek", "given": "Jiri", "initials": "J"}, {"family": "Kallioniemi", "given": "Olli-Pekka", "initials": "OP"}, {"family": "Qian", "given": "Hong", "initials": "H"}, {"family": "Lennartsson", "given": "Andreas", "initials": "A"}, {"family": "Lehmann", "given": "S\u00f6ren", "initials": "S"}], "type": "journal article", "published": "2025-08-23", "journal": {"title": "Cancer Gene Ther", "issn": "1476-5500", "issn-l": null}, "abstract": "As the non-coding genome remains poorly characterized in acute myeloid leukemia (AML), we aimed to identify and functionally characterize novel long non-coding RNAs (lncRNAs) relevant to AML biology and treatment. We first identified lncRNAs overexpressed in AML blasts and, among them, discovered a novel transcript, which we named myeloid and AML-associated intergenic long non-coding RNA (MALNC). MALNC is overexpressed in AML, particularly in cases with the PML-RARA fusion or IDH2R140/NPM1 co-mutations, and is associated with a distinct gene expression profile. Functional studies showed that MALNC knockout impairs AML cell proliferation and colony formation, enhances ATRA-induced differentiation, and sensitizes cells to arsenic trioxide. Transcriptomic analysis revealed that MALNC loss alters the expression of retinoic acid pathway genes, and chromatin binding studies showed that MALNC binds to genes related to the retinoic acid and Rho GTPase pathways. In conclusion, we have identified MALNC as a novel lncRNA that promotes leukemic cell proliferation, counteracts ATRA-induced differentiation, and modulates drug sensitivity in AML.", "doi": "10.1038/s41417-025-00954-0", "pmid": "40849353", "labels": {"NGI Short read": "Service", "NGI Uppsala (SNP&SEQ Technology Platform)": "Service", "National Genomics Infrastructure": "Service", "Bioinformatics Support for Computational Resources": "Service"}, "xrefs": [{"db": "pii", "key": "10.1038/s41417-025-00954-0"}], "notes": [], "created": "2025-09-08T07:03:20.085Z", "modified": "2025-11-14T11:06:29.062Z"}]}