Fibroblast activation protein (FAP), highly expressed in cancer-associated fibroblasts, is closely related to changes in the tumor microenvironment. Radionuclide-labeled FAP inhibitor (FAPI) is a novel tumor therapeutic agent targeting FAP. It can specifically bind to FAP and emit radiation-killing signals, and has been gradually applied to tumor radionuclide internal radiation therapy (IRT). This review summarizes the research progress of various FAP-targeted radiopharmaceuticals in tumor radionuclide IRT, aiming to gain a deeper understanding of their intrinsic properties and promote broader clinical applications.

Fibroblast activation protein (FAP) is overexpressed not only in cancer-associated fibroblasts, but also in bone and joint diseases. With the continuous expansion of the application range of radionuclide labeled FAP inhibitor (FAPI) PET/CT imaging, it has gradually shown a good potential in the clinical diagnosis and efficacy evaluation of bone and joint diseases. This paper reviews the animal and clinical studies of radionuclide-labeled FAPI PET/CT imaging in the diagnosis and treatment of bone and joint diseases like tumors, inflammation, Erdheim-Chester disease (ECD) and so on, aiming to further explore the characteristics of FAPI and expand the scope of clinical application.

The human norepinephrine transporter(hNET)is expressed in neural crest-derived tumors, such as neuroblastoma, pheochromocytoma, and paraganglioma. 18F-meta-fluorobenzylguanidine (MFBG) has high affinity and specificity for hNET, and has been gradually applied to PET/CT imaging in neural crest-derived tumors. The application of 18F-MFBG PET/CT imaging in the diagnosis and treatment of neural crest-derived tumors is reviewed in this article.

Molecular probes targeting the 18×10 3 translocator protein (TSPO) have the ability to identify and monitor tissue inflammation. Their application has expanded from neurological disorders to cardiovascular diseases (CVD), showing promising clinical translational potential in both diagnosis and therapeutic evaluation. This paper introduces the application and value of PET imaging using various generations of TSPO-targeted molecular probes in CVD, including atherosclerosis, acute myocardial infarction, large vessel vasculitis, and others.

BACKGROUND: Bile acids (BAs) facilitate the progression of gastric intestinal metaplasia (GIM). Long non-coding RNAs (lncRNAs) dysregulation was observed along with the initiation of gastric cancer. However, how lncRNAs function in GIM remains unclear. This study aimed to explore the role and mechanism of lncRNA PVT1 in GIM, and provide a potential therapeutic target for GIM treatment. METHODS: We employed RNA sequencing (RNA-seq) to screen dysregulated lncRNAs in gastric epithelial cells after BA treatment. Bioinformatics analysis was conducted to reveal the regulatory mechanism. PVT1 expression was detected in 21 paired biopsies obtained under endoscopy. Overexpressed and knockdown cell models were established to explore gene functions in GIM. Molecular interactions were validated by dual-luciferase reporter assay, RNA immunoprecipitation (RIP), and chromatin immunoprecipitation (Ch-IP). The levels of relative molecular expression were detected in GIM tissues. RESULTS: We confirmed that lncRNA PVT1 was upregulated in BA-induced GIM model. PVT1 promoted the expression of intestinal markers such as CDX2 , KLF4 , and HNF4α . Bioinformatics analysis revealed that miR-34b-5p was a putative target of PVT1 . miR-34b-5p mimics increased CDX2 , KLF4 , and HNF4α levels. Restoration of miR-34b-5p decreased the pro-metaplastic effect of PVT1 . The interactions between PVT1 , miR-34b-5p, and the downstream target HNF4α were validated. Moreover, HNF4α could transcriptionally activated PVT1 , sustaining the GIM phenotype. Finally, the activation of the PVT1 /miR-34b-5p/ HNF4α loop was detected in GIM tissues. CONCLUSIONS BAs facilitate GIM partially via a PVT1/miR-34b-5p/HNF4α positive feedback loop. PVT1 may become a novel target for blocking the continuous development of GIM and preventing the initiation of gastric cancer in patients with bile reflux.
Humans ; RNA, Long Noncoding/metabolism* ; MicroRNAs/metabolism* ; Hepatocyte Nuclear Factor 4/genetics* ; Bile Acids and Salts ; Kruppel-Like Factor 4 ; Metaplasia/metabolism*

Fibroblast activation protein (FAP), highly expressed in cancer-associated fibroblasts, is closely related to changes in the tumor microenvironment. Radionuclide-labeled FAP inhibitor (FAPI) is a novel tumor therapeutic agent targeting FAP. It can specifically bind to FAP and emit radiation-killing signals, and has been gradually applied to tumor radionuclide internal radiation therapy (IRT). This review summarizes the research progress of various FAP-targeted radiopharmaceuticals in tumor radionuclide IRT, aiming to gain a deeper understanding of their intrinsic properties and promote broader clinical applications.

Fibroblast activation protein (FAP) is overexpressed not only in cancer-associated fibroblasts, but also in bone and joint diseases. With the continuous expansion of the application range of radionuclide labeled FAP inhibitor (FAPI) PET/CT imaging, it has gradually shown a good potential in the clinical diagnosis and efficacy evaluation of bone and joint diseases. This paper reviews the animal and clinical studies of radionuclide-labeled FAPI PET/CT imaging in the diagnosis and treatment of bone and joint diseases like tumors, inflammation, Erdheim-Chester disease (ECD) and so on, aiming to further explore the characteristics of FAPI and expand the scope of clinical application.

The human norepinephrine transporter(hNET)is expressed in neural crest-derived tumors, such as neuroblastoma, pheochromocytoma, and paraganglioma. 18F-meta-fluorobenzylguanidine (MFBG) has high affinity and specificity for hNET, and has been gradually applied to PET/CT imaging in neural crest-derived tumors. The application of 18F-MFBG PET/CT imaging in the diagnosis and treatment of neural crest-derived tumors is reviewed in this article.

Molecular probes targeting the 18×10 3 translocator protein (TSPO) have the ability to identify and monitor tissue inflammation. Their application has expanded from neurological disorders to cardiovascular diseases (CVD), showing promising clinical translational potential in both diagnosis and therapeutic evaluation. This paper introduces the application and value of PET imaging using various generations of TSPO-targeted molecular probes in CVD, including atherosclerosis, acute myocardial infarction, large vessel vasculitis, and others.

Objective To investigate the relationship between impaired glucose regulation (IGR) and slow flow or no reflow (SF/NRF) during percutaneous coronary intervention (PCI) in patients with ST segment elevation myocardial infarction (STEMI). Methods Clinical materials of 80 STEMI patients with SF/NRF and 84 STEMI patients without SF/NRF in the hospital from October 2021 to October 2022 were retrospectively collected, including blood glucose, total cholesterol (TC), triglyceride (TG), cardiac troponin Ⅰ (cTnⅠ), fibrinogen, left ventricular ejection fraction (LVEF), D-dimer, uric acid, homocysteine, the ratio of absolute value of neutrophils to absolute value of lymphocytes (NLR), low density lipoprotein cholesterol (LDL-C), high density lipoprotein cholesterol (HDL-C) and 2 h postprandial blood glucose level. Logistic regression model was used to analyze the influencing factors of SF/NRF in STEMI patients with PCI; the receiver operating characteristic (ROC) curve was used to analyze the diagnostic value of fasting blood glucose and 2 h postprandial blood glucose levels for SF/NRF in STEMI patients with PCI. Results Compared with non-SF/NRF group, the levels of cTnⅠ, fibrinogen and HDL-C in SF/NRF group were significantly higher, while the levels of systolic blood pressure (SBP), diastolic blood pressure (DBP) and NLR were significantly lower (P < 0.05). Compared with non-SF/NRF group, the stent diameter, stent length and the time from chest pain to catheter room in SF/NRF group were significantly longer (P < 0.05). The levels of fasting blood glucose and 2 h postprandial blood glucose in SF/NRF group were significantly higher than those in non-SF/NRF group (P < 0.05). Logistic regression analysis showed that fasting blood glucose and 2 h postprandial blood glucose were the influencing factors of SF/NRF in STEMI patients with PCI, and the area under the curve (AUC) of the combination of the two indicators for diagnosis of SF/NRF in STEMI patients during PCI was significantly higher than that by fasting blood glucose and 2 h postprandial blood glucose alone (Z=3.272, 4.369, P < 0.001). Conclusion IGR is related to SF/NRF during PCI in STEMI patients, and fasting blood glucose and 2 h postprandial blood glucose levels are the influencing factors of SF/NRF in STEMI patients.