Subcutaneous Adipose Tissue FDG Uptake is Associated with Systemic Inflammatory Indices Independent of Primary-Tumor Metabolic Burden in Breast Cancer
Molecular Imaging and Biology, 2026 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Basım Tarihi: 2026
- Doi Numarası: 10.1007/s11307-026-02138-0
- Dergi Adı: Molecular Imaging and Biology
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, CINAHL, EMBASE, MEDLINE, Academic Search Ultimate (EBSCO), Natural Science Collection (ProQuest), Biological Science Database (ProQuest), Biomedical Reference Collection: Corporate Edition (EBSCO), Health Research Premium Collection (ProQuest), Materials Science & Engineering Collection (ProQuest), Pharma Collection (ProQuest), Technology Collection (ProQuest)
- Anahtar Kelimeler: 18F-FDG, Abdominal fat, Breast cancer, Inflammation, PET-CT
- İstanbul Üniversitesi Adresli: Evet
Özet
Purpose: Adipose tissue may contribute to systemic inflammation in breast cancer. This study evaluated whether visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) [18F]fluorodeoxyglucose ([18F]FDG) uptakes on positron emission tomography/computed tomography (PET/CT) are associated with inflammatory indices after adjustment for PET-derived tumor metabolic burden and whether metastatic status modifies these associations. Materials and Methods: In this retrospective single-center cohort (n = 358) undergoing baseline [18F]FDG PET/CT, metastatic status was defined using an internal three-level clinical stage grouping: early-stage or locally advanced disease was classified as M0 and metastatic disease was classified as MET. VAT and SAT FDG uptakes were quantified as z-scored mean standardized uptake values normalized to lean body mass (SULmean) using the James lean body mass equation. Inflammatory indices from complete blood counts were log-transformed. Prespecified linear regression models with heteroskedasticity-consistent type 3 (HC3) robust standard errors were adjusted for age, body mass index (BMI), fasting glucose, stage, molecular subtype, and PET-derived primary-tumor metabolic burden metrics. Effect modification was tested via exposure × MET interaction. Sensitivity analyses used total-body tumor burden metrics in MET and recalculated SUL using the Janmahasatian lean body mass equation; overall survival (OS) was explored with Cox models. Results: Of 358 patients, 284 (79.3%) were M0 and 74 (20.7%) were MET. In M0 (complete-case n = 267), higher SAT uptake was independently associated with higher log-transformed neutrophil-to-lymphocyte ratio (log(NLR)) (β = 0.0798; 95% confidence interval (CI) 0.0130–0.1466; p = 0.019). In pooled interaction models (n = 323), SAT remained associated with log(NLR) (β = 0.0892; 95% CI 0.0196–0.1588; p = 0.012; ≈9% higher NLR per 1-standard deviation (SD)), with no evidence of effect modification by metastatic status (SAT × MET interaction p = 0.594). Results were consistent after total-body tumor-burden adjustment in MET and after recalculation of SUL using the Janmahasatian lean body mass equation. SAT was not significantly associated with OS (adjusted hazard ratio (HR) = 1.086; 95% CI 0.864–1.364; p = 0.481; n = 346). Conclusions: Higher SAT FDG uptake was modestly associated with higher NLR independent of tumor metabolic burden, with no evidence of heterogeneity by metastatic status. These findings suggest a potential tissue-specific imaging correlate of host inflammatory phenotype rather than a stand-alone clinical biomarker. Sensitivity and survival analyses remain hypothesis-generating and require external validation.