Pheochromocytomas and paragangliomas (PPGLs) are rare neuroendocrine tumors with metastatic potential. Both 68Ga-DOTATATE and 18F-FDG PET/CT scans have been demonstrated to have important roles in imaging PPGLs, but less is known about the performance of PET/MRI for PPGLs. The study is aimed to investigate whether diffusion-weighted imaging-MRI (DWI-MRI) has an added value to PET imaging in the identification of PPGL lesions by means of integrated PET/MRI.Eleven patients who underwent both 18F-FDG and 68Ga-DOTATATE PET/MRI within 2 weeks were retrospectively included in the study. A total of 56 PPGL lesions were analyzed, and lesion-based detection rates of 68Ga-DOTATATE PET, 18F-FDG PET, DWI-MRI, and PET/MRI were calculated and compared, respectively.68Ga-DOTATATE PET was superior to 18F-FDG PET and DWI-MRI in imaging PPGLs with a lesion-based detection rate of 96.4% (54/56) (95% confidence interval [CI], 87.7%-99.6%), 85.7% (48/56) (95% CI, 76.3%-95.2%), and 89.3% (50/56) (95% CI, 80.9%-97.6%), respectively. PET/MRI with DWI could improve the detection rate of 68Ga-DOTATATE and 18F-FDG PET alone up to 100% in metastatic PPGLs. Lesions of PPGL demonstrated markedly higher tracer uptake in 68Ga-DOTATATE PET than in 18F-FDG PET (P = 0.009 for primary lesion, P = 0.033 for metastases).68Ga-DOTATATE PET showed a higher detection rate than 18F-FDG for PPGLs. In integrated PET/MRI, MRI had an added value to 18F-FDG PET but not much to 68Ga-DOTATATAE PET in identifying PPGL lesions.
To evaluate the utility of 68Ga-DOTATATE and 18F-FDG PET/MR for prediction of grade and stage of pancreatic neuroendocrine tumors (PNETs), and to examine the correlation between parameters obtained from FDG PET and diffusion-weighted imaging (DWI) MR parameters.A retrospective study using 68Ga-DOTATATE and 18F-FDG PET/MR imaging was performed between April 2020 and May 2022 on 46 individuals with histologically confirmed PNETs. Metabolic tumor volume (MTV), maximum standardized uptake value (FSUVmax), and tumor lesion glycolysis (TLG) for FDG; somatostatin receptor density (SRD), maximum standardized uptake value (GSUVmax), and total lesion somatostatin receptor density (TLSRD) for DOTATATE; and minimum and mean apparent diffusion coefficient (ADCmin and ADCmean) values for MRI, respectively. We performed Spearman's correlation analysis to examine the links between these variables and primary tumor stage and grading.Higher PNET grading was associated with higher FSUVmax, MTV, and TLG values (P < 0.05). TLG, SRD, ADCmin, and ADCmean values were correlated with N staging, while SRD, MTV, ADCmin, TLG, and ADCmean were associated with M staging. Notably, ADCmin was a negative correlation between FSUVmax (r = - 0.52; P < 0.001), MTV (r = - 0.50; P < 0.001), and TLG (r = - 0.56; P < 0.001).This study highlights significant correlative relationships between FDG PET-derived parameters and ADCmin. ADCmin may offer utility as a tool for PNET staging and grading in lieu of FDG PET. 68Ga-DOTATATE PET/MR alone may be a sufficient alternative to dual tracer PET/MR when conducting grading and staging of primary PNETs.
Intrinsic emission from nonconjugated polymers has attracted considerable attention owing to its fundamental importance and intensive applications in diverse fields. The emission mechanism, however, is still in debate. Herein, nonconjugated polyacrylonitrile (PAN) molecules are found to be virtually nonluminescent in dilute solutions, while being highly emissive when concentrated or aggregated as nanosuspensions, solid powders, and films, exhibiting distinct aggregation‐induced emission (AIE) characteristics. Moreover, triplet emissions of delayed fluorescence and room temperature phosphorescence are detected from the solid powders. Such unique emission of nonconjugated PAN is ascribed to the formation of cyano clusters, which act as the exact chromophores. In these clusters, through space electronic interactions, namely overlap of π and lone pair (n) electrons among cyano groups extend the conjugation and meanwhile rigidify the molecular conformations, thus offering remarkable emission upon irradiation. The AIE phenomenon can also be well rationalized by the formation of cyano clusters together with conformation rigidification. And the triplet emissions shall be originated from the n–π* transition owing to the presence of lone pairs. It is believed that such clustering‐triggered emission mechanism is instructive for further development of unorthodox luminogens.
Background: Total P16 methylation (P16M), including P16 hydroxymethylation (P16H) and true-P16M, correlates with malignant transformation of oral epithelial dysplasia (OED). Both true-P16M and P16H are early events in carcinogenesis. Aim: The aim of this study is to prospectively determine if discrimination of true-P16M from P16H similarly is necessary for prediction of cancer development from OEDs. Methods: Patients (n = 265) with mild or moderate OED were recruited into the double-blind 2-center cohort. Total-P16M and P16H were analyzed using the 115-bp MethyLight, TET-assistant bisulfite (TAB) methylation-specific PCR (MSP), and TAB-sequencing. Total-P16M-positive and P16H-negative samples were defined as true-P16M-positive. Progression of OEDs was monitored for a minimum 24 months follow-up period. Results: P16H was detected in 23 of 73 (31.5%) total-P16M-positive OEDs. Follow-up information was obtained from 247 patients with an ultimate compliance of 93.2%. OED-derived squamous cell carcinomas were observed in 13.0% (32/247) patients during the follow-up (median, 41.0 months). The cancer progression rate for total-P16M-positive patients was significantly increased when compared with total-P16M-negative patients (23.3% vs 8.6%; adjusted odds ratio = 2.67 [95% CI: 1.19-5.99]). However, the cancer progression rate was similar between P16H- and true-P16M-positive OEDs (26.1% [6/23] vs 22.0% [11/50]; odds ratio = 0.80 [95% CI: 0.22-2.92]). The progression-free survival was also similar for these patients. Conclusion: P16H and true-P16M are similar biomarkers for determining malignant potential of OEDs. Discrimination of P16H from true-P16M, at least in OED, may be not necessary in clinical applications.
The interplay between tumor cells and mesenchymal stem cells (MSCs) within tumor microenvironment plays a significant role in tumor development, and thus might be exploited for therapeutic intervention. In this study, we isolated MSCs from normal gingival tissue (GMSCs), and detected the effect of GMSCs on oral cancer cells via direct co-culture and indirect co-culture systems. The cell proliferation assay of direct co-culture showed that GMSCs could inhibit the growth of oral cancer cells. Conditioned medium derived from GMSCs (GMSCs-CM) also exerted an anticancer effect, which indicates that soluble factors in GMSCs-CM played a dominant role in GMSCs-induced cancer cell growth inhibition. To investigate the mechanism, we performed apoptosis assay by flow cytometry, and confirmed that cancer cell apoptosis induced by GMSCs could be a reason for the effect of GMSCs on the growth of oral cancer cells. Western blotting also confirmed that GMSCs could upregulate expression of pro-apoptotic genes including p-JNK, cleaved PARP, cleaved caspase-3, Bax expression and downregulate proliferation- and anti-apoptosis-related gene expression such as p-ERK1/2, Bcl-2, CDK4, cyclin D1, PCNA and survivin. Importantly, the inhibitory effect of GMSCs on cancer cells can partially be restored by blockade of JNK pathway. Moreover, animal studies showed that GMSCs exerted an anticancer effect after oral cancer cells and GMSCs were co-injected with oral cancer cells. Taken together, our data suggest that GMSCs can suppress oral cancer cell growth in vitro and in vivo via altering the surrounding microenvironment of oral cancer cells, which indicates that GMSCs have a potential use in the management of oral dysplasia and oral cancer in future.
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