Search

Pancreatic cancer is one of the worst prognoses of all malignant tumors, with an annual incidence near its annual mortality rate. To improve the prognosis of patients with pancreatic cancer, it is essential to diagnose and evaluate pancreatic cancer early. Imaging examinations play an essential role in tumor detection, staging, and surgical resection assessment and can provide reliable evidence for the diagnosis and treatment of pancreatic cancer. Currently, imaging techniques commonly used for pancreatic cancer include endoscopic ultrasound (EUS), conventional ultrasound, magnetic resonance imaging (MRI), multidetector spiral computed tomography (MDCT), positron emission tomography/computed tomography (PET/CT), and others PET/CT is a new imaging device composed of PET and CT. 18F-Fluorodeoxyglucose (18F-FDG) is a commonly used tracer in the clinic. Cancer cells are more robust than other ordinary cells in that they can ingest glucose, and the structure of glucose is similar to the structure of 18F-FDG. Therefore, after the injection of 18F-FDG, 18F-FDG in tumor cells appears very thick during PET scanning. Therefore, PET/CT can determine the metabolic capacity and anatomical position of pancreatic tumor cells in the body accurately diagnose the patient's condition and tumor location. It plays a vital role in early diagnosis and accurate staging, predicts survival, and monitors therapeutic effectiveness and pancreatic cancer recurrence. Although 18F-FDG PET/CT has limitations in identifying inflammatory diseases and tumors, it still has good development potential. This article reviews the clinical application of 18F-FDG PET/CT in pancreatic cancer.

Different from surgery, chemical therapy, radio-therapy and target therapy, Chimeric antigen receptor-modified T (CAR-T) cells, a novel adoptive immunotherapy strategy, have been used successfully against both hematological tumors and solid tumors. Although several problems have reduced engineered CAR-T cell therapeutic outcomes in clinical trials for the treatment of thoracic malignancies, including the lack of specific antigens, an immunosuppressive tumor microenvironment, a low level of CAR-T cell infiltration into tumor tissues, off-target toxicity, and other safety issues, CAR-T cell treatment is still full of bright future. In this review, we outline the basic structure and characteristics of CAR-T cells among different period, summarize the common tumor-associated antigens in clinical trials of CAR-T cell therapy for thoracic malignancies, and point out the current challenges and new strategies, aiming to provide new ideas and approaches for preclinical experiments and clinical trials of CAR-T cell therapy for thoracic malignancies.

Introduction Skin cutaneous melanoma (SKCM) is a common skin malignancy worldwide, and its metastasis and mortality rates are high. The molecular characteristics exhibited by tumor-immune interactions have drawn the attention from researchers. Therefore, increased knowledge and new strategies to identify effective immune-related biomarkers may improve the clinical management of SKCM by providing more accurate prognostic information. Patients and methods In this study, we established a prognostic immune-related gene pair (IRGP) signature for predicting the survival of SKCM patients. The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases provided gene expression profiles together with clinical information, and the samples were randomly divided into three groups including the training, testing, and validation datasets. The regression model of least absolute shrinkage and selection operator (LASSO) helped to identify a 13-IRGP signature with a significant relation to the survival of SKCM patients. Results The training, TCGA, and independent sets have an average value of area under the curve of 0.79, 0.76, and 0.82, respectively. In addition, this 13-IRGP signature can noticeably divide SKCM patients into high-risk group and low-risk group with significantly different prognoses. Many biological activities such as gene family were enriched among the genes in our IRGP signature. While analyzing the risk signature and clinical characteristics, there was a large difference in the risk score between T stage and tumor stage grouping. Finally, we constructed a nomogram and forest plots of the risk score and clinical features. Conclusion In summary, we developed a robust 13-IRGP prognostic signature in SKCM, which can identify and provide new insights into immunological biomarkers.

Purpose To evaluate the possible roles of miR-34a expression in thyroid lesions, to unravel the correlation between fluorodeoxyglucose (FDG) uptake and miR-34a expression and moreover, to discover the underlying mechanisms by which miR-34a regulates FDG avidity. Methods We retrospectively reviewed 75 patients with pathology-confirmed thyroid diseases who underwent 18F-FDG positron emission tomography/computed tomography (PET/CT) within 3 months before undergoing thyroid surgery and miR-34a analysis from June 2012 to July 2017. 18F-FDG uptake of thyroid lesions was also analyzed semiquantitatively using maximum standardized uptake value (SUVmax). The association between miR-34a expression and clinicopathological variables (age, sex, TNM stage, histopathology, lesion numbers, location and 18F-FDG avidity) was investigated. When there were multiple lesions in thyroid bed, only the one with the highest 18F-FDG uptake was analyzed. Next, we inhibited the miR-34a expression in TPC-1 cells and detected the expression of glucose transporter 1 (GLUT1) mRNA and protein. Results In the patients cohort, miR-34a was upregulated in those with malignant thyroid diseases compared with benign lesions. The expression of miR-34a was associated with tumor stages, histopathological types and SUVmax. There was an inverse relationship between miR-34a expression and SUVmax in patients with thyroid diseases (Spearman correlation coefficient = -0.553, P < 0.0001). With an SUVmax of 4.3 as the threshold, sensitivity and specificity of the prediction of miR-34a expression (low or high) were 70% and 94.3%, respectively. The area under the receiver operating characteristic curve was 0.843 (95% confidence interval: 0.749, 0.936; P = 0.001). Inhibiting miR-34a in TPC-1 cells significantly increased GLUT1 mRNA and protein expression. Conclusion miR-34a expression was upregulated in thyroid lesions, negatively correlated with SUVmax and can be predicted by FDG SUVmax. In addition, miR-34a may regulate FDG avidity via targeting GLUT1.

[18F]fluoro‑2‑deoxyglucose (FDG) positron emission tomography (PET)‑computed tomography (CT) is a functional imaging modality based on glucose metabolism. The association between the maximum standardized uptake value (SUVmax) from 18F‑FDG PET‑CT scanning and epidermal growth factor receptor (EGFR) mutation status has, to the best of our knowledge, not previously been fully elucidated, and the potential mechanisms by which EGFR mutations alter FDG uptake are largely unknown. A total of 157 patients who were pathologically diagnosed with non‑small cell lung cancer (NSCLC) who underwent EGFR mutation testing and PET‑CT pretreatment between June 2015 and October 2017 were retrospectively analyzed. χ2 and univariate analyses were performed to identify the contributors to EGFR mutation. The receiver operating characteristic (ROC) curve was analyzed, and the area under the curve (AUC) was calculated. Glucose transporter 1 (GLUT1) and NADPH oxidase 4 (NOX4) expression, and reactive oxygen species (ROS) activity were detected in the A549 (wild‑type), PC‑9 (EGFR mutation‑positive, EGFR exon 19del) and NCI‑H1975 (EGFR mutation‑positive, combined with L858R and T790M substitution) cell lines. A total of 109 patients who met the criteria were enrolled, and 63 of those tested as EGFR mutation‑positive. The SUVmax values were significantly lower in patients with EGFR mutations (mean, 6.52±0.38) compared with in patients with wild‑type EGFR (mean, 9.37±0.31; P