{"entity": "journal", "iuid": "1f7bcdd18aca4fd086d9243f19dbdb34", "timestamp": "2026-08-20T20:25:20.810Z", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/journal/Mol%20Cell%20Oncol.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/journal/Mol%20Cell%20Oncol"}}, "title": "Mol Cell Oncol", "issn": "2372-3556", "issn-l": null, "publications_count": 4, "publications": [{"entity": "publication", "iuid": "59b537525af446bb8a9a2fc05ad3f9db", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/59b537525af446bb8a9a2fc05ad3f9db.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/59b537525af446bb8a9a2fc05ad3f9db"}}, "title": "APOBEC3 as a driver of genetic intratumor heterogeneity.", "authors": [{"family": "Venkatesan", "given": "Subramanian", "initials": "S", "orcid": "0000-0001-6454-8508", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/ecacc5d56e504429823daac1d5ea2aeb.json"}}, {"family": "Angelova", "given": "Mihaela", "initials": "M"}, {"family": "Bartkova", "given": "Jirina", "initials": "J"}, {"family": "Bakhoum", "given": "Samuel F", "initials": "SF"}, {"family": "Bartek", "given": "Jiri", "initials": "J"}, {"family": "Kanu", "given": "Nnennaya", "initials": "N"}, {"family": "Swanton", "given": "Charles", "initials": "C"}], "type": "journal article", "published": "2022-01-03", "journal": {"title": "Mol Cell Oncol", "issn": "2372-3556", "volume": "10", "issue": "1", "pages": "2014734", "issn-l": null}, "abstract": "Our recent study revealed that APOBEC3B is upregulated during the preinvasive stages of non-small cell lung cancer and breast cancer. In addition to its role in mediating single nucleotide variants, we propose that APOBEC3 promotes copy number intratumor heterogeneity prior to invasion, providing a substrate for cancer evolution.", "doi": "10.1080/23723556.2021.2014734", "pmid": "38116246", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC10730158"}, {"db": "pii", "key": "2014734"}], "notes": [], "created": "2026-08-20T09:37:52.812Z", "modified": "2026-08-20T09:37:52.873Z"}, {"entity": "publication", "iuid": "eaeb311846cd44cb87eac4d2b38a84c0", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/eaeb311846cd44cb87eac4d2b38a84c0.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/eaeb311846cd44cb87eac4d2b38a84c0"}}, "title": "Targeting tumor vulnerabilities associated with loss of heterozygosity.", "authors": [{"family": "Rendo", "given": "Veronica", "initials": "V", "orcid": "0000-0002-2983-4020", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/9c4c9ca49eb64227be6574a4384ffb46.json"}}, {"family": "Stoimenov", "given": "Ivaylo", "initials": "I", "orcid": "0000-0002-2133-7396", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/10ad1a77c6f241418187734e9a47c16c.json"}}, {"family": "Sj\u00f6blom", "given": "Tobias", "initials": "T"}], "type": "journal article", "published": "2020-05-13", "journal": {"title": "Mol Cell Oncol", "issn": "2372-3556", "volume": "7", "issue": "4", "pages": "1759390", "issn-l": null}, "abstract": "We show that N-acetyltransferase 2 (NAT2) loss of heterozygosity can be targeted in >4% of colorectal cancers with the use of a small molecule. We identify and describe the effect of a compound that impairs the growth of colorectal tumors with slow NAT2 activity by half when compared to wild-type.", "doi": "10.1080/23723556.2020.1759390", "pmid": "32944621", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC7469497"}, {"db": "pii", "key": "1759390"}], "notes": [], "created": "2026-08-20T09:37:51.051Z", "modified": "2026-08-20T09:37:51.114Z"}, {"entity": "publication", "iuid": "239b778e2e954ecf8a5d32bbc4735453", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/239b778e2e954ecf8a5d32bbc4735453.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/239b778e2e954ecf8a5d32bbc4735453"}}, "title": "SAMHD1 is a barrier to antimetabolite-based cancer therapies.", "authors": [{"family": "Rudd", "given": "Sean G", "initials": "SG", "orcid": "0000-0002-4368-3855", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/d65643e96cfe4f3a98cf4f48225eac73.json"}}, {"family": "Schaller", "given": "Torsten", "initials": "T", "orcid": "0000-0001-9597-4112", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/93d3003ec7854be68f4e38283bca1da0.json"}}, {"family": "Herold", "given": "Nikolas", "initials": "N", "orcid": "0000-0001-9468-4543", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/749eedaa5f69414aa315bb875eef9475.json"}}], "type": "journal article", "published": "2017-02-03", "journal": {"title": "Mol Cell Oncol", "issn": "2372-3556", "volume": "4", "issue": "2", "pages": "e1287554", "issn-l": null}, "abstract": "The outcome of acute myelogenous leukemia (AML) therapy depends on the propensity of leukemic blasts to accumulate ara-CTP, the active triphosphate of cytarabine (ara-C). We identified sterile \u03b1 motif and HD domain-containing protein 1 (SAMHD1) as an ara-CTPase that protects cancer cells from cytarabine-induced toxicity. Therefore, we propose targeting SAMHD1 as a strategy to potentiate cytarabine and possibly other antimetabolite-based therapies.", "doi": "10.1080/23723556.2017.1287554", "pmid": "28401188", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC5383367"}, {"db": "pii", "key": "1287554"}], "notes": [], "created": "2026-08-20T09:37:44.566Z", "modified": "2026-08-20T09:37:44.676Z"}, {"entity": "publication", "iuid": "cdb5b1a72f7c489197126f38ed9a948c", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/cdb5b1a72f7c489197126f38ed9a948c.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/cdb5b1a72f7c489197126f38ed9a948c"}}, "title": "Pleiotrophin is a driver of vascular abnormalization in glioblastoma.", "authors": [{"family": "Zhang", "given": "Lei", "initials": "L"}, {"family": "Dimberg", "given": "Anna", "initials": "A"}], "type": "journal article", "published": "2016-02-18", "journal": {"title": "Mol Cell Oncol", "issn": "2372-3556", "volume": "3", "issue": "6", "pages": "e1141087", "issn-l": null}, "abstract": "In a recent report by Zhang et al., pleiotrophin (PTN) was demonstrated to enhance glioma growth by promoting vascular abnormalization. PTN stimulates glioma vessels through anaplastic lymphoma kinase (Alk)-mediated perivascular deposition of vascular endothelial growth factor (VEGF). Targeting of Alk or VEGF signaling normalizes tumor vessels in PTN-expressing tumors.", "doi": "10.1080/23723556.2016.1141087", "pmid": "28090572", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC5160416"}, {"db": "pii", "key": "1141087"}], "notes": [], "created": "2026-08-20T09:37:42.682Z", "modified": "2026-08-20T09:37:42.749Z"}], "created": "2026-08-20T09:37:42.709Z", "modified": "2026-08-20T09:37:42.710Z"}