The advancement of breast cancer therapy is limited by the biologic behaviors of cancer cells, such as metastasis and recurrence. β-adrenoceptors (ADRB) are reported to be associated with the biologic behaviors of breast cancer and may influence glucose metabolism. Here, we sought to investigate the relationship between the activation of ADRB and the expression of glucose transporter (GLUT)-1 and hexokinase (HK)-2 and to clarify the impact of ADRB on ¹⁸F-FDG PET imaging in breast cancer. Methods: ADRB1/2 expression in 4T1, MDA-MB-231, and MCF-7 breast cancer cell lines was detected by Western blotting and immunofluorescence. ADRB-dependent regulation of GLUT-1 and HK-2 was determined by in vitro pharmacologic intervention. 4T1 breast cancer cells were treated with phosphate-buffered saline, isoproterenol, or propranolol, and the transcription and expression of GLUT-1 and HK-2 were measured by quantitative real-time polymerase chain reaction (RT-PCR) and Western blotting, respectively. ADRB1/2 was, respectively, blocked by small-interfering RNA to investigate the direct relationship between ADRB1/2 and HK-2. To evaluate the impact of ADRB on ¹⁸F-FDG PET imaging, BALB/c mice bearing 4T1 tumors were injected with phosphate-buffered saline, isoproterenol, or propranolol, and ¹⁸F-FDG PET imaging was performed. The tumor-to-nontumor (T/NT) values of tumors and brown adipose tissue were calculated by defining the liver as a reference. The in vivo expression of GLUT-1 and HK-2 was observed by immunohistochemical analysis and Western blotting. Results: MDA-MB-231, MCF-7, and 4T1 breast cancer cells were positive for ADRB1/2 expression. The protein expression and posttranscriptional level of HK-2 were significantly decreased by treatment with propranolol in vitro, whereas GLUT-1 expression was not significantly altered by pharmacologic intervention. The expression of HK-2 could be reduced in ADRB2-blocked 4T1 cells. Mice in the propranolol-treated group exhibited lower T/NT values for the tumors and brown adipose tissue than the control group. Immunohistochemical analysis and Western blotting revealed reduced HK-2 expression in the tumors of propranolol-treated mice. Conclusion: The expression of HK-2 was regulated by the activation of ADRB2 in 4T1 breast cancer cells primarily at the posttranscriptional level. Additionally, propranolol prevented glucose metabolism and ¹⁸F-FDG PET imaging of 4T1 breast cancer tumors.

Purpose: The chemokine receptor CXCR4 is overexpressed in various types of human cancers. As a specific imaging agent of CXCR4, ⁶⁸Ga-NOTA-NFB was investigated in this study to assess its safety, biodistribution and dosimetry properties in healthy volunteers, and to preliminarily evaluate its application in glioma patients.

The objectives of this study were to compare the diagnostic potential of ⁶⁸Ga-Alfatide II with¹⁸F-FDG in differentiating between non–small cell lung cancer patients (NSCLC) and lung tuberculosis (TB) patients. Methods: Twenty-one NSCLC patients and 13 TB patients were recruited. PET/CT images using either ⁶⁸Ga-Alfatide II or ¹⁸F-FDG were acquired in 2 consecutive days. SUV quantitative comparison, receiver-operating curve analysis, and comprehensive visual analysis were performed. The expression of the angiogenesis marker α_vβ₃ in NSCLC and TB primary lesions was analyzed by immunohistochemistry. Results: The ⁶⁸Ga-Alfatide II SUV_max and SUV_mean were significantly different in NSCLC and TB (P = 0.0001 and 0.0007, respectively). The area under the receiver-operating curve value of ⁶⁸Ga-Alfatide II SUV_max was significantly higher than that of ¹⁸F-FDG (P = 0.038). The visual differentiation diagnostic specificity of ⁶⁸Ga-Alfatide II was 1.57-fold (84.62% vs. 53.85%) higher than that of ¹⁸F-FDG. In the detection of NSCLC lymph nodes, ⁶⁸Ga-Alfatide II was superior in specificity (100% vs. 66.7%), whereas the sensitivity was greater with ¹⁸F-FDG (87.5% vs. 75%). In TB lymph node detection, the false-positive rate of ⁶⁸Ga-Alfatide II was one-third (15.4%/46.2%) the value of ¹⁸F-FDG. Additionally, ⁶⁸Ga-Alfatide II detected more metastases in the brain but less in the liver and the bone. The α_vβ₃ biomarker was specifically expressed in the cells and the neovasculature of NSCLC lesions. Conclusion: ⁶⁸Ga-Alfatide II is qualified for detecting NSCLC primary lesions and is superior to ¹⁸F-FDG in distinguishing NSCLC from TB in primary lesions and suggestive lymph nodes. ⁶⁸Ga-Alfatide II is more likely to be capable of detecting brain metastasis, and ¹⁸F-FDG is more likely to be capable of detecting liver and early-stage bone metastases.

The study was aimed at assessing the diagnostic performance of ⁶⁸Ga-PSMA-617 PET/CT in the detection of prostate cancer (PCa) in patients with a prostate-specific antigen (PSA) level of 4–20 ng/ml and to compare its efficacy with that of multiparametric MRI (mpMRI). We analyzed the data of 67 consecutive patients with PSA levels of 4–20 ng/ml who almost simultaneously underwent ⁶⁸Ga-PSMA-617 PET/CT and mpMRI. ⁶⁸Ga-PSMA-617 PET/CT and mpMRI diagnostic performances were compared via receiver operating characteristic (ROC) curve analysis. Of the 67 suspected PCa cases, 33 had pathologically confirmed PCa. ⁶⁸Ga-PSMA-617 PET/CT showed a patient-based sensitivity, specificity, and positive and negative predictive values (PPVs and NPVs) of 87.88%, 88.24%, 87.88%, and 88.24%, respectively. The corresponding values for mpMRI were 84.85%, 52.94%, 63.64%, and 78.26%. The area under the curve values for ⁶⁸Ga-PSMA-617 PET/CT and mpMRI were 0.881 and 0.689, respectively. ⁶⁸Ga-PSMA-617 PET/CT showed a better diagnostic performance than mpMRI in the detection of PCa in patients with PSA levels of 4–20 ng/ml.