{"entity": "researcher", "timestamp": "2026-08-20T20:38:53.845Z", "family": "Strauss", "given": "Robert", "initials": "R", "orcid": "0000-0003-1777-7177", "affiliations": ["Genome Integrity Unit, Danish Cancer Society Research Center, Strandboulevarden 49, Copenhagen, DK-2100, Denmark."], "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/researcher/5ac310212e644deba1b8bf8a2a41a705.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/researcher/5ac310212e644deba1b8bf8a2a41a705"}}, "publications": [{"entity": "publication", "iuid": "92b40b92d22e40b2a520241e3e3dd2a3", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/92b40b92d22e40b2a520241e3e3dd2a3.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/92b40b92d22e40b2a520241e3e3dd2a3"}}, "title": "Repurposing Asparaginase Therapy to Target Cisplatin-Resistant Cancer Cells.", "authors": [{"family": "Wang", "given": "Jiantao", "initials": "J"}, {"family": "Pouryaghoub", "given": "Nasim", "initials": "N"}, {"family": "Strauss", "given": "Robert", "initials": "R", "orcid": "0000-0003-1777-7177", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/5ac310212e644deba1b8bf8a2a41a705.json"}}, {"family": "Bartek", "given": "Jiri", "initials": "J"}, {"family": "Zhang", "given": "Si Min", "initials": "SM"}, {"family": "Rudd", "given": "Sean G", "initials": "SG", "orcid": "0000-0002-4368-3855", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/d65643e96cfe4f3a98cf4f48225eac73.json"}}], "type": "journal article", "published": "2025-10-00", "journal": {"title": "Fundam Clin Pharmacol", "issn": "1472-8206", "volume": "39", "issue": "5", "pages": "e70044", "issn-l": null}, "abstract": "Cisplatin and its derivatives remain a cornerstone in the treatment of solid malignancies. Resistance is a major factor limiting their clinical utility.\n\nIn the present study, we set out to interrogate therapeutic approaches to target cisplatin-resistant cancer cells. We focused on therapies exploiting metabolic pathways that are altered in drug-resistant cells. We sought to find an existing therapy that has monotherapy efficacy against cisplatin-resistant cancer cells that can also re-sensitize to cisplatin.\n\nWe used lung and ovarian cancer cell lines with acquired resistance to cisplatin together with drug sensitivity assays, conducted both with monotherapies and cisplatin combinations.\n\nWe show that cancer cell lines with acquired resistance to cisplatin have altered levels of enzymes involved in glutamine metabolism, which can result in differential sensitivity to targeted agents. We show that expression of one of these enzymes-the glutamate-cystine antiporter SLC7A11, up-regulated 6-fold in a cisplatin-resistant lung cancer cell line-has potential prognostic significance in lung cancer but not ovarian cancer. After identifying a common dependency of cisplatin-resistant cancer cells upon extracellular glutamine, we then evaluate the utility of the long-standing anti-leukemic therapy asparaginase (ASNase)-which possesses both asparaginase and glutaminase activity-as a potential approach. We show ASNase preferentially inhibits the proliferation of cisplatin-resistant cancer cells and can potentially re-sensitize these cells to cisplatin.\n\nOur results underpin the prevalence of altered metabolism in cisplatin-resistant cells and highlight the potential utility of re-purposing ASNase to target these cells, warranting further investigation.", "doi": "10.1111/fcp.70044", "pmid": "40784667", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC12335911"}], "notes": [], "created": "2026-08-20T11:17:50.563Z", "modified": "2026-08-20T11:17:50.663Z"}, {"entity": "publication", "iuid": "35507cf3450745f497420acc2010ae06", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/35507cf3450745f497420acc2010ae06.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/35507cf3450745f497420acc2010ae06"}}, "title": "Glutamine-addiction in cisplatin resistant cancer cells is mediated by SLC7A11 and can be targeted with asparaginase therapy", "authors": [{"family": "Wang", "given": "Jiantao", "initials": "J", "orcid": "0000-0001-6397-9429", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/736395487707411b80d10ef2dd597168.json"}}, {"family": "Strauss", "given": "Robert", "initials": "R", "orcid": "0000-0003-1777-7177", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/5ac310212e644deba1b8bf8a2a41a705.json"}}, {"family": "Bartek", "given": "Jiri", "initials": "J", "orcid": "0000-0003-2013-7525", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/288939950c0c4c6393d35c84e5128b5f.json"}}, {"family": "Rudd", "given": "Sean G", "initials": "SG", "orcid": "0000-0002-4368-3855", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/d65643e96cfe4f3a98cf4f48225eac73.json"}}], "type": "posted-content", "published": "2024-07-22", "journal": {"issn-l": null}, "abstract": null, "doi": "10.1101/2024.07.19.604261", "pmid": null, "labels": [], "xrefs": [], "notes": [], "created": "2026-08-20T10:55:44.095Z", "modified": "2026-08-20T10:55:44.226Z"}, {"entity": "publication", "iuid": "600f53f40ed949aca32306d8a05d8075", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/600f53f40ed949aca32306d8a05d8075.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/600f53f40ed949aca32306d8a05d8075"}}, "title": "SPT6-driven error-free DNA repair safeguards genomic stability of glioblastoma cancer stem-like cells.", "authors": [{"family": "Obara", "given": "Elisabeth Anne Adanma", "initials": "EAA"}, {"family": "Aguilar-Morante", "given": "Diana", "initials": "D", "orcid": "0000-0001-9775-0841", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/3666f8a0020e4b2c8f34edefb81c4084.json"}}, {"family": "Rasmussen", "given": "Rikke Darling", "initials": "RD"}, {"family": "Frias", "given": "Alex", "initials": "A"}, {"family": "Vitting-Serup", "given": "Kristoffer", "initials": "K"}, {"family": "Lim", "given": "Yi Chieh", "initials": "YC", "orcid": "0000-0003-1261-5419", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/305e71771ac54fb399ae5467a8e4a4b7.json"}}, {"family": "Elb\u00e6k", "given": "Kirstine Juul", "initials": "KJ"}, {"family": "Pedersen", "given": "Henriette", "initials": "H"}, {"family": "Vardouli", "given": "Lina", "initials": "L"}, {"family": "Jensen", "given": "Kamilla Ellermann", "initials": "KE"}, {"family": "Skjoth-Rasmussen", "given": "Jane", "initials": "J"}, {"family": "Brennum", "given": "Jannick", "initials": "J"}, {"family": "Tuckova", "given": "Lucie", "initials": "L"}, {"family": "Strauss", "given": "Robert", "initials": "R", "orcid": "0000-0003-1777-7177", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/5ac310212e644deba1b8bf8a2a41a705.json"}}, {"family": "Dinant", "given": "Christoffel", "initials": "C"}, {"family": "Bartek", "given": "Jiri", "initials": "J"}, {"family": "Hamerlik", "given": "Petra", "initials": "P", "orcid": "0000-0002-5856-0161", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/e4f53a4f82f84c0395cf527c88157517.json"}}], "type": "journal article", "published": "2020-09-18", "journal": {"title": "Nat Commun", "issn": "2041-1723", "volume": "11", "issue": "1", "pages": "4709", "issn-l": "2041-1723"}, "abstract": "Glioblastoma cancer-stem like cells (GSCs) display marked resistance to ionizing radiation (IR), a standard of care for glioblastoma patients. Mechanisms underpinning radio-resistance of GSCs remain largely unknown. Chromatin state and the accessibility of DNA lesions to DNA repair machineries are crucial for the maintenance of genomic stability. Understanding the functional impact of chromatin remodeling on DNA repair in GSCs may lay the foundation for advancing the efficacy of radio-sensitizing therapies. Here, we present the results of a high-content siRNA microscopy screen, revealing the transcriptional elongation factor SPT6 to be critical for the genomic stability and self-renewal of GSCs. Mechanistically, SPT6 transcriptionally up-regulates BRCA1 and thereby drives an error-free DNA repair in GSCs. SPT6 loss impairs the self-renewal, genomic stability and tumor initiating capacity of GSCs. Collectively, our results provide mechanistic insights into how SPT6 regulates DNA repair and identify SPT6 as a putative therapeutic target in glioblastoma.", "doi": "10.1038/s41467-020-18549-8", "pmid": "32948765", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC7501306"}, {"db": "pii", "key": "10.1038/s41467-020-18549-8"}], "notes": [], "created": "2026-08-20T08:51:11.476Z", "modified": "2026-08-20T08:51:11.665Z"}, {"entity": "publication", "iuid": "ce532e4a42ea4ef889bce43c57b8d295", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/ce532e4a42ea4ef889bce43c57b8d295.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/ce532e4a42ea4ef889bce43c57b8d295"}}, "title": "Daughters sense their mother's stress.", "authors": [{"family": "Strauss", "given": "Robert", "initials": "R", "orcid": "0000-0003-1777-7177", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/5ac310212e644deba1b8bf8a2a41a705.json"}}, {"family": "Bartek", "given": "Jiri", "initials": "J", "orcid": "0000-0003-2013-7525", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/288939950c0c4c6393d35c84e5128b5f.json"}}], "type": "news", "published": "2018-01-10", "journal": {"title": "Cell Cycle", "issn": "1551-4005", "volume": "17", "issue": "2", "pages": "145-146", "issn-l": null}, "abstract": null, "doi": "10.1080/15384101.2017.1408235", "pmid": "29192544", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC5884352"}], "notes": [], "created": "2026-08-20T09:36:46.786Z", "modified": "2026-08-20T09:36:46.843Z"}]}