{"entity": "journal", "iuid": "69ef70776aca48ccbc1930feaec5e37a", "timestamp": "2026-04-13T04:32:01.944Z", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/journal/J%20Clin%20Oncol.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/journal/J%20Clin%20Oncol"}}, "title": "J Clin Oncol", "issn": "1527-7755", "issn-l": "0732-183X", "publications_count": 2, "publications": [{"entity": "publication", "iuid": "367da52594d24257b0893c583572611c", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/367da52594d24257b0893c583572611c.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/367da52594d24257b0893c583572611c"}}, "title": "Clonal Hematopoiesis and Risk of Incident Lung Cancer.", "authors": [{"family": "Tian", "given": "Ruiyi", "initials": "R", "orcid": "0000-0001-5024-6832", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/1a2cc8a38bbe41649a441405def87345.json"}}, {"family": "Wiley", "given": "Brian", "initials": "B"}, {"family": "Liu", "given": "Jie", "initials": "J", "orcid": "0000-0001-6365-1888", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/ddad30666cdd405aa37bb60d42f29348.json"}}, {"family": "Zong", "given": "Xiaoyu", "initials": "X", "orcid": "0000-0001-5646-710X", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/f1250f735b6b4cd2a6873a9208e862a8.json"}}, {"family": "Truong", "given": "Buu", "initials": "B", "orcid": "0000-0003-0043-0812", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/24e9ec70c1f74fdfa182de3d7d9e21fa.json"}}, {"family": "Zhao", "given": "Stephanie", "initials": "S", "orcid": "0000-0001-6637-1486", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/e8551483c0f5406b864d2353e8978add.json"}}, {"family": "Uddin", "given": "Md Mesbah", "initials": "MM", "orcid": "0000-0003-1846-0411", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/42f1ac7010c34ba997a3fd9e56c6a56a.json"}}, {"family": "Niroula", "given": "Abhishek", "initials": "A", "orcid": "0000-0002-5904-0635", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/05df7afc7a494ba5af8a378e5ffa53f0.json"}}, {"family": "Miller", "given": "Christopher A", "initials": "CA", "orcid": "0000-0003-4266-6700", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/80d153aa89554327b42354faae946064.json"}}, {"family": "Mukherjee", "given": "Semanti", "initials": "S", "orcid": "0000-0002-1843-9359", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/7fe7a9badb944aa5998031b33a6d43cc.json"}}, {"family": "Heiden", "given": "Brendan T", "initials": "BT", "orcid": "0000-0002-0116-7377", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/9fa032b03f8b4b9cab62d43a2d4fc7ac.json"}}, {"family": "Luo", "given": "Jingqin", "initials": "J", "orcid": "0000-0003-2759-3072", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/767ef98656bb42149d14aebb4618059e.json"}}, {"family": "Puri", "given": "Varun", "initials": "V"}, {"family": "Kozower", "given": "Benjamin D", "initials": "BD"}, {"family": "Walter", "given": "Matthew J", "initials": "MJ", "orcid": "0000-0002-7753-1091", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/055099b1d98c4b43bf1163a4553c1f34.json"}}, {"family": "Ding", "given": "Li", "initials": "L"}, {"family": "Link", "given": "Daniel C", "initials": "DC"}, {"family": "Amos", "given": "Christopher I", "initials": "CI", "orcid": "0000-0002-8540-7023", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/dc5439b0cf4b4619a56d6d361fc12210.json"}}, {"family": "Ebert", "given": "Benjamin L", "initials": "BL", "orcid": "0000-0003-0197-5451", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/56e4f1c53a4348e2b0ceb44a38850a17.json"}}, {"family": "Govindan", "given": "Ramaswamy", "initials": "R", "orcid": "0000-0002-6964-9612", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/f0d884b2cbfb41af8df1101ba9d7f7d0.json"}}, {"family": "Natarajan", "given": "Pradeep", "initials": "P", "orcid": "0000-0001-8402-7435", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/fe8bd48c61c047cd8e61c35d9e9ac650.json"}}, {"family": "Bolton", "given": "Kelly L", "initials": "KL", "orcid": "0000-0001-6584-3357", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/74eb7c71cebc4e8c888ff2b7426b4438.json"}}, {"family": "Cao", "given": "Yin", "initials": "Y", "orcid": "0000-0001-9835-7662", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/a34eb276a5514342adb104aa5df642c9.json"}}], "type": "journal article", "published": "2023-03-01", "journal": {"title": "J Clin Oncol", "issn": "1527-7755", "volume": "41", "issue": "7", "pages": "1423-1433", "issn-l": "0732-183X"}, "abstract": "To prospectively examine the association between clonal hematopoiesis (CH) and subsequent risk of lung cancer.\n\nAmong 200,629 UK Biobank (UKBB) participants with whole-exome sequencing, CH was identified in a nested case-control study of 832 incident lung cancer cases and 3,951 controls (2006-2019) matched on age and year at blood draw, sex, race, and smoking status. A similar nested case-control study (141 cases/652 controls) was conducted among 27,975 participants with whole-exome sequencing in the Mass General Brigham Biobank (MGBB, 2010-2021). In parallel, we compared CH frequency in published data from 5,003 patients with solid tumor (2,279 lung cancer) who had pretreatment blood sequencing performed through Memorial Sloan Kettering-Integrated Mutation Profiling of Actionable Cancer Targets.\n\nIn UKBB, the presence of CH was associated with increased risk of lung cancer (cases: 12.5% v controls: 8.7%; multivariable-adjusted odds ratio [OR], 1.36; 95% CI, 1.06 to 1.74). The association remained robust after excluding participants with chronic obstructive pulmonary disease. No significant interactions with known risk factors, including polygenic risk score and C-reactive protein, were identified. In MGBB, we observed similar enrichment of CH in lung cancer (cases: 15.6% v controls: 12.7%). The meta-analyzed OR (95% CI) of UKBB and MGBB was 1.35 (1.08 to 1.68) for CH overall and 1.61 (1.19 to 2.18) for variant allele frequencies \u2265 10%. In Memorial Sloan Kettering-Integrated Mutation Profiling of Actionable Cancer Targets, CH with a variant allele frequency \u2265 10% was enriched in pretreatment lung cancer compared with other tumors after adjusting for age, sex, and smoking (OR for lung v breast cancer: 1.61; 95% CI, 1.03 to 2.53).\n\nIndependent of known risk factors, CH is associated with increased risk of lung cancer.", "doi": "10.1200/JCO.22.00857", "pmid": "36480766", "labels": {"Abhishek Niroula": null, "DDLS Fellow": null}, "xrefs": [{"db": "pmc", "key": "PMC9995101"}], "notes": [], "created": "2023-11-20T11:36:22.458Z", "modified": "2023-11-20T11:36:23.254Z"}, {"entity": "publication", "iuid": "2edf76c162e744ee9e75c122934963b1", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/2edf76c162e744ee9e75c122934963b1.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/2edf76c162e744ee9e75c122934963b1"}}, "title": "Integrating the \"Immunome\" in the Stratification of Myelodysplastic Syndromes and Future Clinical Trial Design.", "authors": [{"family": "Winter", "given": "Susann", "initials": "S"}, {"family": "Shoaie", "given": "Saeed", "initials": "S"}, {"family": "Kordasti", "given": "Shahram", "initials": "S"}, {"family": "Platzbecker", "given": "Uwe", "initials": "U"}], "type": "journal article", "published": "2020-05-20", "journal": {"title": "J Clin Oncol", "issn": "1527-7755", "issn-l": "0732-183X", "volume": "38", "issue": "15", "pages": "1723-1735"}, "abstract": "Myelodysplastic syndromes (MDS) are characterized by ineffective hematopoiesis and often include a dysregulation and dysfunction of the immune system. In the context of population aging, MDS incidence is set to increase substantially, with exponential increases in health care costs, given the limited and expensive treatment options for these patients. Treatment selection is mainly based on calculated risk categories according to a Revised International Prognostic Scoring System (IPSS-R). However, although IPSS-R is an excellent predictor of disease progression, it is an ineffective predictor of response to disease-modifying therapies. Redressing these unmet needs, the \"immunome\" is a key, multifaceted component in the initiation and overall response against malignant cells in MDS, and the current omission of immune status monitoring may in part explain the insufficiencies of current prognostic stratification methods. Nevertheless, integrating these and other recent molecular advances into clinical practice proves difficult. This review highlights the complexity of immune dysregulation in MDS pathophysiology and the fine balance between smoldering inflammation, adaptive immunity, and somatic mutations in promoting or suppressing malignant clones. We review the existing knowledge and discuss how state-of-the-art immune monitoring strategies could potentially permit novel patient substratification, thereby empowering practical predictions of response to treatment in MDS. We propose novel multicenter studies, which are needed to achieve this goal.", "doi": "10.1200/JCO.19.01823", "pmid": "32058844", "labels": {"Saeed Shoaie": null, "SciLifeLab Fellow": null}, "xrefs": [], "notes": [], "created": "2020-11-26T14:21:41.872Z", "modified": "2022-11-04T11:32:14.981Z"}], "created": "2020-11-26T14:21:41.883Z", "modified": "2020-11-27T13:12:54.951Z"}