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Updated: Aug 6, 2026
Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer
Published on: July 21, 2018
Smoking reshapes systemic metabolic coordination across lung cancer subtypes: a multicenter total-body 18F-FDG PET/CT
Haiyan Wang1,2,3, Yaping Wu4, Yanhua Duan5
1Biomedical Imaging Laboratory (BIG), Department of Electrical and Computer Engineering, Faculty of Science and Technology, University of Macau, Taipa, Macau SAR, 999078, China.
Purpose:
Lung cancer (LC) is increasingly recognized as a systemic disease, and these systemic alterations may differ across histological subtypes. Smoking is a major risk factor for LC, yet its impact on systemic metabolism across LC subtypes remains underexplored.
Methods:
We studied 125 LC patients and 200 healthy controls from three centers who underwent static and dynamic total-body 18F-FDG PET/CT. Thirty-seven regions of interest spanning the central nervous system and peripheral organs were analyzed. Regional standardized uptake values normalized by lean body mass and time-activity curves were harmonized using ComBat and adjusted for demographic covariates. Population-level metabolic networks were constructed from bootstrapped Pearson correlations of regional uptake to characterize smoking status-associated systemic alterations across LC subtypes. Individual-level metabolic networks were derived from correlations of residual time-activity curves after third-order polynomial fitting, from which organ-specific abnormality strength metrics were calculated. In addition, tumor habitats were defined from PET/CT intensity and entropy features, and their associations with smoking status and organ-level abnormalities were assessed using multivariable regression analyses.
Results:
Population- and individual-level network analyses showed that smoking status was associated with altered systemic metabolic coordination in a subtype-dependent manner, with the liver consistently emerging as a central hub of metabolic disruption. Tumor habitat analysis further revealed a smoking-associated shift toward hypometabolic tumor microenvironments.
Conclusion:
These findings provide quantitative insight into smoking status-related systemic metabolic reprogramming in LC and highlight the potential value of imaging-based characterization across histological subtypes.
