{"entity": "researcher", "timestamp": "2026-08-20T21:22:34.301Z", "family": "Johnsen", "given": "John Inge", "initials": "JI", "orcid": "0000-0003-1277-812X", "affiliations": ["Department of Women's and Children's Health, Karolinska Institutet, 171 76 Stockholm, Sweden."], "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/researcher/e63aa6bb0fba481abeb58c2f1568b3c9.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/researcher/e63aa6bb0fba481abeb58c2f1568b3c9"}}, "publications": [{"entity": "publication", "iuid": "6c010782909544428eedd71a8172bc70", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/6c010782909544428eedd71a8172bc70.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/6c010782909544428eedd71a8172bc70"}}, "title": "MYCMI-7: A Small MYC-Binding Compound that Inhibits MYC: MAX Interaction and Tumor Growth in a MYC-Dependent Manner.", "authors": [{"family": "Castell", "given": "Alina", "initials": "A"}, {"family": "Yan", "given": "Qinzi", "initials": "Q"}, {"family": "Fawkner", "given": "Karin", "initials": "K"}, {"family": "Bazzar", "given": "Wesam", "initials": "W"}, {"family": "Zhang", "given": "Fan", "initials": "F", "orcid": "0000-0002-9782-3016", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/75a11bf01f11481d813b282b3ded3508.json"}}, {"family": "Wickstr\u00f6m", "given": "Malin", "initials": "M", "orcid": "0000-0001-5214-9956", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/338ea31865c44e0d86a9947dbed04a28.json"}}, {"family": "Alzrigat", "given": "Mohammad", "initials": "M", "orcid": "0000-0001-5514-8625", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/602febc530284c0790edbd2d1f4aa734.json"}}, {"family": "Franco", "given": "Marcela", "initials": "M"}, {"family": "Krona", "given": "Cecilia", "initials": "C"}, {"family": "Cameron", "given": "Donald P", "initials": "DP"}, {"family": "Dyberg", "given": "Cecilia", "initials": "C"}, {"family": "Olsen", "given": "Thale Kristin", "initials": "TK"}, {"family": "Verschut", "given": "Vasiliki", "initials": "V"}, {"family": "Schmidt", "given": "Linn\u00e9a", "initials": "L"}, {"family": "Lim", "given": "Sheryl Y", "initials": "SY", "orcid": "0000-0002-2606-9220", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/1cc385947d5c492a9b37bccefdef5414.json"}}, {"family": "Mahmoud", "given": "Loay", "initials": "L"}, {"family": "Hydbring", "given": "Per", "initials": "P"}, {"family": "Lehmann", "given": "S\u00f6ren", "initials": "S"}, {"family": "Baranello", "given": "Laura", "initials": "L", "orcid": "0000-0001-6039-1849", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/249ce47702914b009281dde6c8ef402d.json"}}, {"family": "Nelander", "given": "Sven", "initials": "S"}, {"family": "Johnsen", "given": "John Inge", "initials": "JI", "orcid": "0000-0003-1277-812X", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/e63aa6bb0fba481abeb58c2f1568b3c9.json"}}, {"family": "Larsson", "given": "Lars-Gunnar", "initials": "LG", "orcid": "0000-0001-6914-3147", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/5ec1f8f2738a41cb9105c142ca5374e6.json"}}], "type": "journal article", "published": "2022-03-00", "journal": {"title": "Cancer Res Commun", "issn": "2767-9764", "volume": "2", "issue": "3", "pages": "182-201", "issn-l": null}, "abstract": "Deregulated expression of MYC family oncogenes occurs frequently in human cancer and is often associated with aggressive disease and poor prognosis. While MYC is a highly warranted target, it has been considered \"undruggable,\" and no specific anti-MYC drugs are available in the clinic. We recently identified molecules named MYCMIs that inhibit the interaction between MYC and its essential partner MAX. Here we show that one of these molecules, MYCMI-7, efficiently and selectively inhibits MYC:MAX and MYCN:MAX interactions in cells, binds directly to recombinant MYC, and reduces MYC-driven transcription. In addition, MYCMI-7 induces degradation of MYC and MYCN proteins. MYCMI-7 potently induces growth arrest/apoptosis in tumor cells in a MYC/MYCN-dependent manner and downregulates the MYC pathway on a global level as determined by RNA sequencing. Sensitivity to MYCMI-7 correlates with MYC expression in a panel of 60 tumor cell lines and MYCMI-7 shows high efficacy toward a collection of patient-derived primary glioblastoma and acute myeloid leukemia (AML) ex vivo cultures. Importantly, a variety of normal cells become G1 arrested without signs of apoptosis upon MYCMI-7 treatment. Finally, in mouse tumor models of MYC-driven AML, breast cancer, and MYCN-amplified neuroblastoma, treatment with MYCMI-7 downregulates MYC/MYCN, inhibits tumor growth, and prolongs survival through apoptosis with few side effects. In conclusion, MYCMI-7 is a potent and selective MYC inhibitor that is highly relevant for the development into clinically useful drugs for the treatment of MYC-driven cancer.\n\nOur findings demonstrate that the small-molecule MYCMI-7 binds MYC and inhibits interaction between MYC and MAX, thereby hampering MYC-driven tumor cell growth in culture and in vivo while sparing normal cells.", "doi": "10.1158/2767-9764.CRC-21-0019", "pmid": "36874405", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC9980915"}, {"db": "pii", "key": "CRC-21-0019"}], "notes": [], "created": "2026-08-20T12:14:47.464Z", "modified": "2026-08-20T12:14:47.824Z"}, {"entity": "publication", "iuid": "8fe4a1d767fc4ad7bc41eb58710cc1bd", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/8fe4a1d767fc4ad7bc41eb58710cc1bd.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/8fe4a1d767fc4ad7bc41eb58710cc1bd"}}, "title": "Modeling SHH-driven medulloblastoma with patient iPS cell-derived neural stem cells.", "authors": [{"family": "Susanto", "given": "Evelyn", "initials": "E"}, {"family": "Marin Navarro", "given": "Ana", "initials": "A"}, {"family": "Zhou", "given": "Leilei", "initials": "L"}, {"family": "Sundstr\u00f6m", "given": "Anders", "initials": "A", "orcid": "0000-0003-3942-6271", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/63e6602d2807417684239b93eb065a26.json"}}, {"family": "van Bree", "given": "Niek", "initials": "N", "orcid": "0000-0001-5010-3524", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/afdb3d47b0be46cbbf7e10f7367f6d7b.json"}}, {"family": "Stantic", "given": "Marina", "initials": "M"}, {"family": "Moslem", "given": "Mohsen", "initials": "M", "orcid": "0000-0002-2440-9586", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/ac548b831c044a53ac324691083df9e1.json"}}, {"family": "Tailor", "given": "Jignesh", "initials": "J"}, {"family": "Rietdijk", "given": "Jonne", "initials": "J"}, {"family": "Zubillaga", "given": "Veronica", "initials": "V", "orcid": "0000-0002-8806-939X", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/0feb462e3293492bae0e051990b387df.json"}}, {"family": "H\u00fcbner", "given": "Jens-Martin", "initials": "JM"}, {"family": "Weishaupt", "given": "Holger", "initials": "H"}, {"family": "Wolfsberger", "given": "Johanna", "initials": "J"}, {"family": "Alafuzoff", "given": "Irina", "initials": "I", "orcid": "0000-0002-6249-569X", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/0d5a2e976bc84739a957f2b12517df7e.json"}}, {"family": "Nordgren", "given": "Ann", "initials": "A"}, {"family": "Magnaldo", "given": "Thierry", "initials": "T", "orcid": "0000-0001-9174-8599", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/09542eee2b7748769298e9d4fcdc5a22.json"}}, {"family": "Siesj\u00f6", "given": "Peter", "initials": "P"}, {"family": "Johnsen", "given": "John Inge", "initials": "JI", "orcid": "0000-0003-1277-812X", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/e63aa6bb0fba481abeb58c2f1568b3c9.json"}}, {"family": "Kool", "given": "Marcel", "initials": "M", "orcid": "0000-0002-6557-5468", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/da81ade40cfb45329b5ef3a190834913.json"}}, {"family": "Tammimies", "given": "Kristiina", "initials": "K", "orcid": "0000-0002-8324-4697", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/480cdbabfc57460f967e6921f12e6ec4.json"}}, {"family": "Darabi", "given": "Anna", "initials": "A", "orcid": "0000-0003-4326-8149", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/bb9f19a0c8694ee79ca515a79976d146.json"}}, {"family": "Swartling", "given": "Fredrik J", "initials": "FJ", "orcid": "0000-0002-8460-4367", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/2e673fa8c86348fb8c1a2ae34ba7ba9a.json"}}, {"family": "Falk", "given": "Anna", "initials": "A", "orcid": "0000-0003-1634-8610", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/4a8825c33511418a83eceffdb530dadb.json"}}, {"family": "Wilhelm", "given": "Margareta", "initials": "M", "orcid": "0000-0002-0516-9724", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/b22feedd1d3c464ba7d8f6635fb00826.json"}}], "type": "journal article", "published": "2020-08-18", "journal": {"title": "Proc. Natl. Acad. Sci. U.S.A.", "issn": "1091-6490", "volume": "117", "issue": "33", "pages": "20127-20138", "issn-l": "0027-8424"}, "abstract": "Medulloblastoma is the most common malignant brain tumor in children. Here we describe a medulloblastoma model using Induced pluripotent stem (iPS) cell-derived human neuroepithelial stem (NES) cells generated from a Gorlin syndrome patient carrying a germline mutation in the sonic hedgehog (SHH) receptor PTCH1. We found that Gorlin NES cells formed tumors in mouse cerebellum mimicking human medulloblastoma. Retransplantation of tumor-isolated NES (tNES) cells resulted in accelerated tumor formation, cells with reduced growth factor dependency, enhanced neurosphere formation in vitro, and increased sensitivity to Vismodegib. Using our model, we identified LGALS1 to be a GLI target gene that is up-regulated in both Gorlin tNES cells and SHH-subgroup of medulloblastoma patients. Taken together, we demonstrate that NES cells derived from Gorlin patients can be used as a resource to model medulloblastoma initiation and progression and to identify putative targets.", "doi": "10.1073/pnas.1920521117", "pmid": "32747535", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC7443968"}, {"db": "pii", "key": "1920521117"}], "notes": [], "created": "2026-08-20T09:30:35.661Z", "modified": "2026-08-20T09:30:36.075Z"}]}