scholarly journals 18F-fludrodeoxyglucose maximal standardized uptake value and metabolic tumor burden are associated with major chemotherapy-related tumor markers in NSCLC patients

2016 ◽  
Vol Volume 9 ◽  
pp. 6315-6324 ◽  
Author(s):  
Lu Bai ◽  
Chihua Guo ◽  
Jiansheng Wang ◽  
Xiang Liu ◽  
Yang Li ◽  
...  
2020 ◽  
Author(s):  
Wen-qiang Zheng ◽  
Puhong Zhang ◽  
Bin Quan ◽  
Guang-jian Gao ◽  
Qing Chen ◽  
...  

Abstract Background: Non-small cell lung (NSCLC) holds high mortality owing to the difficulty to early detection from other lung mass, such as tuberculosis. This study evaluates the clinical value of the combination of circulating cell-free DNA (cfDNA) quantification and metabolic tumor burden to distinguish NSCLC from tuberculosis. Methods: A total of 149 NSCLC patients, 151 tuberculosis patients and 150 healthy controls were included. Quantifying serum cfDNA fragments from ALU (115 bp) gene by RT-PCR. Metabolic tumor burden (SUV-Maxa) values were detected by preoperative the 18F-fluorodeoxyglucose positron emission tomography (18F-FDG PET/CT). A549 cell, NCI–H460 cell, NSCLC and tuberculosis mice model were used to elucidate the specific mechanism. Results: Serum cfDNA levels and SUV-Maxa were higher in NSCLC patients than those in healthy controls and those in tuberculosis. Meanwhile, mice models showed the similar discovery. In addition, obvious correlations of cfDNA and metabolic tumor burden were only existed in NSCLC patients and mice model, rather than tuberculosis and control. Moreover, the combination of cfDNA and metabolic tumor burden displayed better effect to distinguish NSCLC from tuberculosis than alone use. Mechanistically, upregulated Glucose transporter 1 (GLU1) increased necroptosis-induce cfDNA rise by FasL/caspase 8/caspase 3 pathway and promoted metabolic tumor burden in NSCLC. Conclusions: The combination of cfDNA and metabolic tumor burden displayed better effect to distinguish NSCLC from tuberculosis, owing to upregulated GLU1 increased cfDNA levels by FasL/caspase 8/caspase 3 pathways and promoted metabolic tumor burden in NSCLC.


2015 ◽  
Vol 360 (2) ◽  
pp. 227-233 ◽  
Author(s):  
Si Shi ◽  
Shunrong Ji ◽  
Yi Qin ◽  
Jin Xu ◽  
Bo Zhang ◽  
...  

Lung Cancer ◽  
2016 ◽  
Vol 94 ◽  
pp. 81-87 ◽  
Author(s):  
Anne Winther-Larsen ◽  
Joan Fledelius ◽  
Boe Sandahl Sorensen ◽  
Peter Meldgaard

2021 ◽  
Author(s):  
Wen-qiang Zheng ◽  
Puhong Zhang ◽  
Bin Quan ◽  
Guang-jian Gao ◽  
Qing Chen ◽  
...  

Abstract Background: Non-small cell lung (NSCLC) holds high mortality owing to the difficulty to early detection from other lung mass, such as tuberculosis. This study evaluates the clinical value of the combination of circulating cell-free DNA (cfDNA) quantification and metabolic tumor burden to distinguish NSCLC from tuberculosis. Methods: A total of 149 NSCLC patients, 151 tuberculosis patients and 150 healthy controls were included. Quantifying serum cfDNA fragments from ALU (115 bp) gene by RT-PCR. Metabolic tumor burden (SUV-Maxa) values were detected by preoperative the 18F-fluorodeoxyglucose positron emission tomography (18F-FDG PET/CT). A549 cell, NCI–H460 cell, NSCLC and tuberculosis mice model were used to elucidate the specific mechanism. Results: Serum cfDNA levels and SUV-Maxa were higher in NSCLC patients than those in healthy controls and those in tuberculosis. Meanwhile, mice models showed the similar discovery. In addition, obvious correlations of cfDNA and metabolic tumor burden were only existed in NSCLC patients and mice model, rather than tuberculosis and control. Moreover, the combination of cfDNA and metabolic tumor burden displayed better effect to distinguish NSCLC from tuberculosis than alone use. Mechanistically, upregulated Glucose transporter 1 (GLU1) increased necroptosis-induce cfDNA rise by FasL/caspase 8/caspase 3 pathway and promoted metabolic tumor burden in NSCLC. Conclusions: The combination of cfDNA and metabolic tumor burden displayed better effect to distinguish NSCLC from tuberculosis, owing to upregulated GLU1 increased cfDNA levels by FasL/caspase 8/caspase 3 pathways and promoted metabolic tumor burden in NSCLC.


Pathogens ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 839
Author(s):  
Tzu-Chuan Ho ◽  
Chin-Chuan Chang ◽  
Hung-Pin Chan ◽  
Ying-Fong Huang ◽  
Yi-Ming Arthur Chen ◽  
...  

During the coronavirus disease 2019 (COVID-19) pandemic, several case studies demonstrated that many asymptomatic patients with COVID-19 underwent fluorine-18 fluorodeoxyglucose ([18F]FDG) positron emission tomography/computed tomography (PET/CT) examination for various indications. However, there is a lack of literature to characterize the pattern of [18F]FDG PET/CT imaging on asymptomatic COVID-19 patients. Therefore, a systematic review to analyze the pulmonary findings of [18F]FDG PET/CT on asymptomatic COVID-19 patients was conducted. This systematic review was performed under the guidelines of PRISMA. PubMed, Medline, and Web of Science were used to search for articles for this review. Articles with the key words: “asymptomatic”, “COVID-19”, “[18F]FDG PET/CT”, and “nuclear medicine” were searched for from 1 January 2020 to 20 May 2021. Thirty asymptomatic patients with COVID-19 were included in the eighteen articles. These patients had a mean age of 62.25 ± 14.85 years (male: 67.71 ± 12.00; female: 56.79 ± 15.81). [18F]FDG-avid lung lesions were found in 93.33% (28/30) of total patients. The major lesion was [18F]FDG-avid multiple ground-glass opacities (GGOs) in the peripheral or subpleural region in bilateral lungs, followed by the consolidation. The intensity of [18F]FDG uptake in multiple GGOs was 5.605 ± 2.914 (range from 2 to 12) for maximal standardized uptake value (SUVmax). [18F]FDG-avid thoracic lymph nodes (LN) were observed in 40% (12/40) of the patients. They mostly appeared in both mediastinal and hilar regions with an SUVmax of 5.8 ± 2.93 (range from 2.5 to 9.6). The [18F]FDG uptake was observed in multiple GGOs, as well as in the mediastinal and hilar LNs. These are common patterns in PET/CT of asymptomatic patients with COVID-19.


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