Introduction/Background The aim of this study was to explore abdominal fat distribution markers from computed tomography (CT) in relation to clinicopathologic characteristics and patient outcome in uterine cervical cancer (CC). By unravelling possible links between fat distribution profiles and altered tumour signalling pathways, potential molecular targets for treatment based on body composition profiles may be identified, which may enable more individualized treatment strategies in CC.
Methodology The study included 316 CC patients diagnosed during 2004–2017 who had pre-treatment abdominal CT scans. CT images were analysed to quantify total abdominal fat volume (TAV), subcutaneous abdominal fat volume (SAV), visceral abdominal fat volume (VAV), visceral fat percentage (VAV% = VAV/TAV x100), liver density (LD) and waist circumference (WC). CT morphometric markers were explored in relation to clinicopathologic characteristics and disease-specific survival (DSS), and to gene expression profiles (L1000 mRNA) in a subset of 108 patients.
Results High TAV, VAV and VAV% and low LD were all associated with high (≥44 years) patient age (p≤0.017) and high International Federation of Gynaecology and Obstetrics (FIGO) (2018) stage (p≤0.01). High VAV% was the only CT marker predicting high-grade histology (p=0.028), large tumour size (p=0.016) and poor DSS (HR 1.06, p<0.001). VAV% was strongly positively correlated with age (r=0.68, p<0.001) and VAV (r=0.65, p<0.001). Patients with high VAV% had CC tumours with enrichment of gene sets (false discovery rate [FDR] <5%) related to inflammatory signalling with 65% (13/20) of the top ranked Gene Ontology gene sets related to interferon signalling, viral- or immune response.
Conclusion High VAV% is associated with high-risk clinical features and predicts reduced disease-specific survival in CC patients. CC patients with high VAV% have tumours with upregulated genes involved in inflammatory signalling, suggesting that the metabolic environment induced by visceral adiposity influences the regulatory signalling pathways relevant for tumour progression in CC.
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