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We investigated whether genetic susceptibility to tuberculosis (TB) influences lung adenocarcinoma development among never-smokers using TB genome-wide association study (GWAS) results within the Female Lung Cancer Consortium in Asia. Pathway analysis with the adaptive rank truncated product method was used to assess the association between a TB-related gene-set and lung adenocarcinoma using GWAS data from 5512 lung adenocarcinoma cases and 6277 controls. The gene-set consisted of 31 genes containing known/suggestive associations with genetic variants from previous TB-GWAS. Subsequently, we followed-up with Mendelian Randomization to evaluate the association between TB and lung adenocarcinoma using three genome-wide significant variants from previous TB-GWAS in East Asians. The TB-related gene-set was associated with lung adenocarcinoma (p = 0.016). Additionally, the Mendelian Randomization showed an association between TB and lung adenocarcinoma (OR = 1.31, 95% CI: 1.03, 1.66, p = 0.027). Our findings support TB as a causal risk factor for lung cancer development among never-smoking Asian women.
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http://dx.doi.org/10.1016/j.ygeno.2019.07.008 | DOI Listing |
Br J Cancer
September 2025
Department of Genetics, Institut Curie, PSL Research University, Paris, France.
Background: Identifying molecular alterations specific to advanced lung adenocarcinomas could provide insights into tumour progression and dissemination mechanisms.
Method: We analysed tumour samples, either from locoregional lesions or distant metastases, from patients with advanced lung adenocarcinoma from the SAFIR02-Lung trial by targeted sequencing of 45 cancer genes and comparative genomic hybridisation array and compared them to early tumours samples from The Cancer Genome Atlas.
Results: Differences in copy-number alterations frequencies suggest the involvement in tumour progression of LAMB3, TNN/KIAA0040/TNR, KRAS, DAB2, MYC, EPHA3 and VIPR2, and in metastatic dissemination of AREG, ZNF503, PAX8, MMP13, JAM3, and MTURN.
Cancer Sci
September 2025
Section of Oncopathology and Morphological Pathology, Department of Pathology, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.
Low-density lipoprotein receptor-related protein 11 (LRP11) is reported to be overexpressed in various cancers; however, its functional role in lung adenocarcinoma remains poorly understood. This study aimed to elucidate the tumor-promoting function of LRP11 in lung adenocarcinoma. We assessed the expression and function of LRP11 in lung adenocarcinoma cell lines through both silencing and overexpression experiments.
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September 2025
Department of Epidemiology, School of Public Health, and Key Laboratory of Public Health Safety of Ministry of Education, Fudan University, Shanghai, China
Objectives: Although lung cancer in never smokers (LCNSs) accounts for an estimated 25% of all lung cancer cases, the temporal trends in LCNS incidence and its broader epidemiological patterns remain poorly understood. Our study examines the temporal trends in LCNS incidence and analyses key epidemiological characteristics, specifically, the trends in mortality rates, survival rates and changes in age at onset to illuminate the reasons for temporal trends in LCNS incidence.
Design: Retrospective population-based cohort study.
J Thorac Oncol
September 2025
Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam, Republic of Korea; Emeritus Professor, Seoul National University College of Medicine, Seoul, Republic of Korea.
Introduction: Multifocal subsolid nodules (SSNs) are increasingly detected with widespread lung cancer screening and advanced thoracic imaging, representing a spectrum of multifocal lung adenocarcinomas (LUADs). When synchronous SSNs coexist with a surgically confirmed subsolid LUAD, their trajectories remain poorly understood, contributing to uncertainty regarding optimal management strategies. This study aimed to evaluate the clinical course and impact of synchronous SSNs in such patients and to identify features associated with their progression.
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September 2025
Department of Clinical Laboratory, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200030, China; Shanghai Institute of Thoracic Oncology, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200030, China; Faculty of Medical Laborat
Cytokines link inflammation to tumorigenesis, but the role of post-translational modifications in regulating their function within the extra-tumoral environment remains poorly defined. Here, we identify tumor-derived tumor necrosis factor (TNF) receptor superfamily member 11B (TR11B) as a key driver of lung adenocarcinoma (LUAD) progression and therapeutic resistance. Mechanistically, O-GlcNAc transferase (OGT)-mediated O-GlcNAcylation at serine 151 stabilizes TR11B and facilitates its interaction with the membrane protein EPS15 homology domain-containing protein 1 (EHD1), promoting cyclin dependent kinase 2 (CDK2) phosphorylation and cell cycle progression.
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