Kim TH, et al. J Gastric Cancer. 2023 Jan;23:e11. https://doi.org/10.5230/jgc.2023.23.e11

Despite the favorable prognosis of stage IA non–small cell lung cancer (NSCLC), the disease recurs after complete surgical resection in 20%–30% of patients. This study determined the prognostic value of various metabolic parameters of ¹⁸F-FDG PET/CT in surgically resected stage IA NSCLC. Methods: We retrospectively reviewed 248 patients with stage IA NSCLC who underwent lobectomy and complete lymph node dissection after PET/CT. A region of interest was drawn on the primary lesion, and metabolic indices such as metabolic tumor volume, maximum standardized uptake value (SUV_max), and total lesion glycolysis (TLG) were measured using an SUV cutoff of 2.5. Results: The patients included 134 men and 114 women, and the mean age was 63.03 ± 10.01 y; 129 were stage T1a (≤2 cm) and 119 were T1b (>2 cm). The median follow-up period was 36.6 mo. Recurrence took place in 15 patients. The mean (±SD) SUV_max, metabolic tumor volume, and TLG were 4.55 ± 3.75, 5.92 ± 5.57, and 14.42 ± 17.35, respectively. The cutoffs of SUV_max and TLG were 3.7 and 13.76, respectively. The 5-y overall survival (OS) was 95.1% in low-SUV_max patients and 82.2% in high-SUV_max patients (P = 0.02). The 5-y OS was 93.7% in low-TLG patients and 78.3% in high-TLG patients (P = 0.01). On multivariate analysis, TLG was a risk factor for OS (hazard ratio, 3.159; P = 0.040), but SUV_max showed marginal significance (P = 0.064). The concordance index of the TLG model was 0.676 (95% CI, 0.541–0.812). Conclusion: TLG was a significant prognostic factor for OS in patients with stage IA NSCLC.

Purpose: We investigated the prognostic effect of incorporating metabolic assessment by ¹⁸F-fluoro-2-deoxyglucose uptake on positron emission tomography/computed tomography (¹⁸F-FDG-PET/CT) into a conventional staging system in small-cell lung cancer (SCLC). Experimental Design: Seventy-six consecutive patients with pathologically proven SCLC were enrolled. All patients underwent standard treatment after pretreatment ¹⁸F-FDG-PET/CT scanning. The mean values of maximal standardized uptake values (meanSUV_max) of the malignant lesions upon ¹⁸F-FDG-PET/CT were calculated. The Cox proportional hazards model was used with performance status, lactate dehydrogenase, stage, and meanSUV_max. Results: Patients with high meanSUV_max were significantly related with the established poor prognostic factors, such as higher lactate dehydrogenase (P = 0.04) and extensive disease (ED; P = 0.01). Furthermore, in multivariate analysis, patients with high meanSUV_max were associated with poor survival outcomes compared with patients with low meanSUV_max [adjusted hazard ratio, 3.74; 95% confidence interval (95% CI), 1.67-8.37; P = 0.001, for death and adjusted hazard ratio, 2.25; 95% CI, 1.21-4.17; P = 0.01 for recurrence/progression]. In subgroup analysis, limited disease (LD) with high meanSUV_max showed significantly shorter overall survival than LD with low meanSUV_max [high versus low meanSUV_max, 20.1 months (95% CI, 7.9-23.2) versus 35.3 months (95% CI, 27.6-42.9); P = 0.02]. ED with high meanSUV_max had significantly shorter overall survival than ED with low meanSUV_max [high versus low meanSUV_max, 9.5 months (95% CI, 4.9-13.9) versus 17.7 months (95% CI, 12.0-20.1); P = 0.007]. These findings were replicated in progression-free survival analysis. Conclusions: In SCLC, tumor metabolic activity as assessed by FDG-PET is a significant prognostic factor and identifies subgroups of patients at higher risk of death in both LD and ED SCLC.

To assess the utility of F-18 fluorodeoxyglucose positron emission tomography/computed tomography (FDG PET/CT) in evaluating pancreatic intraductal papillary mucinous neoplasm (IPMN). We included 31 patients with pancreatic IPMN who underwent F-18 FDG PET/CT and multidetector CT (MDCT). Each pancreatic lesion was classified as benign or malignant. On PET, the maximal standardized uptake value was measured in each pancreatic lesion. PET/CT was superior to MDCT in diagnosing malignant IPMN. All 22 concordant results gave accurate diagnoses. Of 9 discordant results, MDCT misdiagnosed 7 IPMNs, whereas PET/CT misinterpreted 2. Malignant IPMNs showed significantly higher maximal standardized uptake values (mean ± standard deviation, 6.7 ± 3.6) than benign IPMNs (mean ± standard deviation, 2.1 ± 1.0) (P Conclusions: F-18 FDG PET/CT outperformed MDCT in detecting malignant IPMN.

EGFR mutation-induced cell proliferation causes changes in tumor biology and tumor metabolism, which may reflect tumor marker concentration and 18F-FDG uptake on PET/CT. Direct aspirates of primary lung tumors contain different concentrations of tumor markers than serum tumor markers, and may correlate better with EGFR mutation than serum tumor markers. The purpose of this study is to investigate an association between cytologic tumor markers and FDG uptake with EGFR mutation status in non-small cell lung cancer (NSCLC). We prospectively collected tumor aspirates of 61 patients who underwent EGFR mutation analysis. Serum and cytologic CYFRA 21-1, CEA, and SCCA levels were measured and correlated with EGFR gene mutations. FDG PET/CT was performed on 58 patients for NSCLC staging, and SUV was correlated with EGFR mutation status. Thirty (50 %) patients had EGFR mutation and 57 patients had adenocarcinoma subtype. Univariate analysis showed that female gender, never smoker, high levels of cytologic CYFRA 21-1 (c-CYFRA) and lower maximum standard uptake value (SUVmax) were correlated with EGFR mutations. ROC generated cut-off values of 20.8 ng/ml for c-CYFRA and SUVmax of 9.6 showed highest sensitivity for EGFR mutation detection. Multivariate analysis revealed that female gender [hazard ratio (HR): 18.15, p = 0.025], higher levels of c-CYFRA (HR: 7.58, and lower SUVmax (HR: 0.08, p = 0.005) were predictive of harboring EGFR mutation. The cytologic tumor marker c-CYFRA was positively associated with EGFR mutations in NSCLC. EGFR mutation-positive NSCLCs have relatively lower glycolysis compared with NSCLCs without EGFR mutation.