{"entity": "researcher", "timestamp": "2026-03-10T03:06:59.525Z", "family": "Tobin", "given": "Nicholas P", "initials": "NP", "orcid": "0000-0003-2343-9772", "affiliations": ["Department of Oncology and Pathology, Karolinska Institutet and University Hospital, Stockholm, Sweden. nick.tobin@ki.se."], "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/researcher/b9aa223903694c8399b89adc231facce.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/researcher/b9aa223903694c8399b89adc231facce"}}, "publications": [{"entity": "publication", "iuid": "8143db0e550e4134b2ef07c0a4e06d6a", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/8143db0e550e4134b2ef07c0a4e06d6a.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/8143db0e550e4134b2ef07c0a4e06d6a"}}, "title": "Reclassifying tumour cell cycle activity in terms of its tissue of origin.", "authors": [{"family": "Lundberg", "given": "Arian", "initials": "A", "orcid": "0000-0002-6630-2787", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/baa2c7c8963840bfb6a22d7c5cfe35f9.json"}}, {"family": "Yi", "given": "Joan Jong Jing", "initials": "JJJ", "orcid": "0000-0002-4735-301X", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/6e2eda77a9e04bef8400ddb96fdba325.json"}}, {"family": "Lindstr\u00f6m", "given": "Linda S", "initials": "LS"}, {"family": "Tobin", "given": "Nicholas P", "initials": "NP", "orcid": "0000-0003-2343-9772", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/b9aa223903694c8399b89adc231facce.json"}}], "type": "journal article", "published": "2022-08-20", "journal": {"title": "NPJ Precis Oncol", "issn": "2397-768X", "volume": "6", "issue": "1", "pages": "59", "issn-l": null}, "abstract": "Genomic alterations resulting in loss of control over the cell cycle is a fundamental hallmark of human malignancies. Whilst pan-cancer studies have broadly assessed tumour genomics and their impact on oncogenic pathways, analyses taking the baseline signalling levels in normal tissue into account are lacking. To this end, we aimed to reclassify the cell cycle activity of tumours in terms of their tissue of origin and determine if any common DNA mutations, chromosome arm-level changes or signalling pathways contribute to an increase in baseline corrected cell cycle activity. Combining normal tissue and pan-cancer data from over 13,000 samples we demonstrate that tumours of gynaecological origin show the highest levels of corrected cell cycle activity, partially owing to hormonal signalling and gene expression changes. We also show that normal and tumour tissues can be separated into groups (quadrants) of low/high cell cycle activity and propose the hypothesis of an upper limit on these activity levels in tumours.", "doi": "10.1038/s41698-022-00302-7", "pmid": "35987928", "labels": {"DDLS Fellow": null, "Arian Lundberg": null}, "xrefs": [{"db": "pmc", "key": "PMC9392789"}, {"db": "pii", "key": "10.1038/s41698-022-00302-7"}], "notes": [], "created": "2025-11-14T07:51:47.320Z", "modified": "2026-01-03T12:21:55.200Z"}, {"entity": "publication", "iuid": "c15d49242f7b4a60a9d76b23e514d949", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/c15d49242f7b4a60a9d76b23e514d949.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/c15d49242f7b4a60a9d76b23e514d949"}}, "title": "A pan-cancer analysis of the frequency of DNA alterations across cell cycle activity levels.", "authors": [{"family": "Lundberg", "given": "Arian", "initials": "A", "orcid": "0000-0002-6630-2787", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/baa2c7c8963840bfb6a22d7c5cfe35f9.json"}}, {"family": "Lindstr\u00f6m", "given": "Linda S", "initials": "LS"}, {"family": "Parker", "given": "Joel S", "initials": "JS", "orcid": "0000-0003-2080-6901", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/586d6382c81c407983976de4de3c9835.json"}}, {"family": "L\u00f6verli", "given": "Elinor", "initials": "E"}, {"family": "Perou", "given": "Charles M", "initials": "CM", "orcid": "0000-0001-9827-2247", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/3f7179d8a91d4703ae5bdfa3e003f941.json"}}, {"family": "Bergh", "given": "Jonas", "initials": "J"}, {"family": "Tobin", "given": "Nicholas P", "initials": "NP", "orcid": "0000-0003-2343-9772", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/b9aa223903694c8399b89adc231facce.json"}}], "type": "journal article", "published": "2020-08-00", "journal": {"title": "Oncogene", "issn": "1476-5594", "volume": "39", "issue": "32", "pages": "5430-5440", "issn-l": "0950-9232"}, "abstract": "Pan-cancer genomic analyses based on the magnitude of pathway activity are currently lacking. Focusing on the cell cycle, we examined the DNA mutations and chromosome arm-level aneuploidy within tumours with low, intermediate and high cell-cycle activity in 9515 pan-cancer patients with 32 different tumour types. Boxplots showed that cell-cycle activity varied broadly across and within all cancers. TP53 and PIK3CA mutations were common in all cell cycle score (CCS) tertiles but with increasing frequency as cell-cycle activity levels increased (P < 0.001). Mutations in BRAF and gains in 16p were less frequent in CCS High tumours (P < 0.001). In Kaplan-Meier analysis, patients whose tumours were CCS Low had a longer Progression Free Interval (PFI) relative to Intermediate or High (P < 0.001) and this significance remained in multivariable analysis (CCS Intermediate: HR = 1.37; 95% CI 1.17-1.60, CCS High: 1.54; 1.29-1.84, CCS Low = Ref). These results demonstrate that whilst similar DNA alterations can be found at all cell-cycle activity levels, some notable exceptions exist. Moreover, independent prognostic information can be derived on a pan-cancer level from a simple measure of cell-cycle activity.", "doi": "10.1038/s41388-020-1367-4", "pmid": "32581248", "labels": {"DDLS Fellow": null, "Arian Lundberg": null}, "xrefs": [{"db": "mid", "key": "NIHMS1702965"}, {"db": "pmc", "key": "PMC8159764"}, {"db": "pii", "key": "10.1038/s41388-020-1367-4"}], "notes": [], "created": "2025-11-14T07:51:50.036Z", "modified": "2025-11-14T07:51:50.187Z"}, {"entity": "publication", "iuid": "fef3a5d364cf48299a854fb7fe8081fa", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/fef3a5d364cf48299a854fb7fe8081fa.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/fef3a5d364cf48299a854fb7fe8081fa"}}, "title": "The long-term prognostic and predictive capacity of cyclin D1 gene amplification in 2305 breast tumours.", "authors": [{"family": "Lundberg", "given": "Arian", "initials": "A", "orcid": "0000-0002-6630-2787", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/baa2c7c8963840bfb6a22d7c5cfe35f9.json"}}, {"family": "Lindstr\u00f6m", "given": "Linda S", "initials": "LS"}, {"family": "Li", "given": "Jingmei", "initials": "J"}, {"family": "Harrell", "given": "J Chuck", "initials": "JC"}, {"family": "Darai-Ramqvist", "given": "Eva", "initials": "E"}, {"family": "Sifakis", "given": "Emmanouil G", "initials": "EG"}, {"family": "Foukakis", "given": "Theodoros", "initials": "T"}, {"family": "Perou", "given": "Charles M", "initials": "CM"}, {"family": "Czene", "given": "Kamila", "initials": "K"}, {"family": "Bergh", "given": "Jonas", "initials": "J"}, {"family": "Tobin", "given": "Nicholas P", "initials": "NP", "orcid": "0000-0003-2343-9772", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/b9aa223903694c8399b89adc231facce.json"}}], "type": "journal article", "published": "2019-02-28", "journal": {"title": "Breast Cancer Res.", "issn": "1465-542X", "volume": "21", "issue": "1", "pages": "34", "issn-l": "1465-5411"}, "abstract": "Use of cyclin D1 (CCND1) gene amplification as a breast cancer biomarker has been hampered by conflicting assessments of the relationship between cyclin D1 protein levels and patient survival. Here, we aimed to clarify its prognostic and treatment predictive potential through comprehensive long-term survival analyses.\n\nCCND1 amplification was assessed using SNP arrays from two cohorts of 1965 and 340 patients with matching gene expression array and clinical follow-up data of over 15 years. Kaplan-Meier and multivariable Cox regression analyses were used to determine survival differences between CCND1 amplified vs. non-amplified tumours in clinically relevant patient sets, within PAM50 subtypes and within treatment-specific subgroups. Boxplots and differential gene expression analyses were performed to assess differences between amplified vs. non-amplified tumours within PAM50 subtypes.\n\nWhen combining both cohorts, worse survival was found for patients with CCND1-amplified tumours in luminal A (HR = 1.68; 95% CI, 1.15-2.46), luminal B (1.37; 1.01-1.86) and ER+/LN-/HER2- (1.66; 1.14-2.41) subgroups. In gene expression analysis, CCND1-amplified luminal A tumours showed increased proliferation (P < 0.001) and decreased progesterone (P = 0.002) levels along with a large overlap in differentially expressed genes when comparing luminal A and B-amplified vs. non-amplified tumours.\n\nOur results indicate that CCND1 amplification is associated with worse 15-year survival in ER+/LN-/HER2-, luminal A and luminal B patients. Moreover, luminal A CCND1-amplified tumours display gene expression changes consistent with a more aggressive phenotype. These novel findings highlight the potential of CCND1 to identify patients that could benefit from long-term treatment strategies.", "doi": "10.1186/s13058-019-1121-4", "pmid": "30819233", "labels": {"DDLS Fellow": null, "Arian Lundberg": null}, "xrefs": [{"db": "pmc", "key": "PMC6394106"}, {"db": "pii", "key": "10.1186/s13058-019-1121-4"}], "notes": [], "created": "2025-11-14T07:51:51.389Z", "modified": "2026-01-03T12:43:33.474Z"}]}