Kim S, et al. Yonsei Med J. 2023 May;64(5):320-326. https://doi.org/10.3349/ymj.2022.0548

Purpose: This retrospective study aimed to correlate ¹⁸F-FDG uptake on PET/CT with isocitrate dehydrogenase enzyme isoform 1 (IDH1) mutation in patients with cerebral gliomas. Hierarchical interactions between factors affecting overall survival (OS) were also examined. Methods: In 59 patients with glioma, the ratio of the SUVmax of a glioma to the SUVmean of the contralateral cortex (G/C ratio) on ¹⁸F-FDG PET/CT and the presence of IDH1 mutation were correlated. The prognostic value of clinicopathologic factors and G/C ratio for OS were assessed using a Cox proportional hazards model and classification and regression tree models. Results: The mean G/C ratio of IDH1-mutant tumors was significantly lower than that of IDH1 wild-type tumors (0.73 vs 1.14, P = 0.004). In multivariate analysis, IDH1-mutant and G/C ratio were significant for OS. The classification and regression tree modeling identified 3 risk groups for OS (group 1: IDH1 mutant [hazard ratio, 0.2]; group 2: G/C ratio ≤0.8 with IDH1 wild type [hazard ratio, 0.83]; group 3: G/C ratio >0.8 with IDH1 wild type [hazard ratio, 1.9]) (overall P < 0.001). The mean OS was 37.0 months in group 1, 28.6 months in group 2, and 20.7 months in group 3, respectively, showing significant differences among the groups (group 1 vs group 2: P = 0.023, group 2 vs group 3: P = 0.049, group 1 vs group3: P < 0.001). Conclusions: ¹⁸F-FDG uptake of IDH1-mutant gliomas was significantly lower than that of IDH1 wild-type gliomas. IDH1 mutation was the most important factor in identifying patients with the best prognosis, whereas increased ¹⁸F-FDG uptake provided additional prognostic information for predicting poor OS among patients with IDH1 wild-type gliomas.

Background/Objectives: Pulmonary fibrosis is a progressive and fatal lung disease with limited diagnostic and therapeutic options. Fibroblast activation protein (FAP) has emerged as a promising molecular imaging target for the non-invasive assessment of fibrotic activity. This study aimed to evaluate the diagnostic feasibility of [⁶⁸Ga]Ga-FAP inhibitor (FAPI) and [¹⁸F]fluorodeoxyglucose ([¹⁸F]FDG) positron emission tomography (PET) for imaging pulmonary fibrosis in a mouse model. Methods: A pulmonary fibrosis model was established by intratracheal administration of polyhexamethylene guanidine-phosphate (PHMG-p) to C57BL/6 mice. Fibrosis severity was quantified by the Ashcroft scoring system using hematoxylin and eosin and Masson’s trichrome staining and evaluated by computed tomography (CT) imaging at 7, 14, and 21 days after PHMG-p exposure. PET imaging was performed, and ex vivo biodistribution was assessed after injection of [⁶⁸Ga]Ga-FAPI-04 and [¹⁸F]FDG. Results: Histological analysis and Ashcroft scoring revealed greater fibrosis severity in the PHMG-p-treated group. Western blot analysis demonstrated upregulation of FAP expression after PHMG-p exposure. CT showed increased mean lung density, while [⁶⁸Ga]Ga-FAPI-04 PET revealed significantly elevated pulmonary uptake of [⁶⁸Ga]Ga-FAPI-04 in the PHMG-p-treated group compared with the controls. [¹⁸F]FDG PET imaging also showed higher uptake of [¹⁸F]FDG in the PHMG-p-treated group than in the controls. Ex vivo biodistribution confirmed greater [⁶⁸Ga]Ga-FAPI-04 accumulation in the lungs of PHMG-p-treated mice. Conclusions: [⁶⁸Ga]Ga-FAPI-04 PET serves as a sensitive imaging biomarker for evaluation of fibrotic activity in PHMG-p-induced pulmonary fibrosis and complements [¹⁸F]FDG PET for assessing disease progression and therapeutic response.