Aim: To evaluate whether positron emission tomography (PET) with ¹⁸F-2-deoxyglucose (FDG) can detect pelvic lymph node metastases in prostate cancer patients who had elevated serum prostate-specific antigen (PSA) levels after treatment. Methods: Twenty-four patients with a rising serum PSA level after treatment for localized prostate cancer were examined with FDG-PET before pelvic lymph node dissection. All patients had negative findings on whole body bone scan and equivocal pelvic computed tomography (CT) results. The results of FDG-PET were then compared to the histology of the pelvic lymph nodes obtained at surgery. Results: Lymph node metastases were detected by histopathological examination in 16/24 (66.7%) patients. At the sites with histopathologically proven metastases, increased FDG uptake was found in 12/16 (75.0%) patients. In addition, there were 4 patients with false-negative results, but no patient with a false-positive result on FDG-PET images. The sensitivity, specificity, accuracy, positive predictive value, and negative predictive value of FDG-PET in detecting metastatic pelvic lymph nodes were 75.0, 100.0, 83.3, 100.0, and 67.7%, respectively. Conclusions: These results suggest that FDG-PET may be a valuable diagnostic tool in the staging of pelvic lymph nodes in patients with PSA relapse after treatment of localized prostate cancer when the whole body bone scan is negative and pelvic CT findings are equivocal.

MALDI-TOF spectrometry has not been used for urinary exosome analysis. We used it for determining UC biomarkers. From 2012 to 2015, we enrolled 129 consecutive patients with UC and 62 participants without UC. Exosomes from their urine were isolated, and analyzed through MALDI-TOF spectrometry. Immunohistochemical (IHC) analysis of another 122 UC and 26 non-UC tissues was conducted to verify the discovered biomarkers. Two peaks at m/z 5593 (fragmented peptide of alpha-1-antitrypsin; sensitivity, 50.4%; specificity, 96.9%) and m/z 5947 (fragmented peptide of histone H2B1K sensitivity, 62.0%; specificity, 92.3%) were identified as UC diagnosis exosome biomarkers. UC patients with detectable histone H2B1K showed 2.29- and 3.11-fold increased risks of recurrence and progression, respectively, compared with those with nondetectable histone H2B1K. Verification results of IHC staining revealed significantly higher expression of alpha 1-antitrypsin (p = 0.038) and H2B1K (p = 0.005) in UC tissues than in normal tissues. The expression of alpha 1-antitrypsin and H2B1K in UC tissues was significantly correlated with UC grades (p < 0.05). Urinary exosome proteins alpha 1-antitrypsin and histone H2B1K, which are identified through MALDI-TOF analysis, could facilitate rapid diagnosis and prognosis of UC.

This study examines the role of IGF2/mannose 6-phosphate receptor (IGF2R) signaling in the signaling transduction regulation and cell apoptosis in H9c2 cardiomyoblast cells. However, it is difficult to recognize the distinct activation of IGF2 signaling without interfacing with IGFI receptor (IGF1R) after exposure to IGF2. Leu27IGF2, an analog of IGF2 that interacts selectively with the IGF2R, was used to specifically activate IGF2R signaling in this study. DNA fragmentation and TUNEL assay revealed that in contrast to IGF1 treatment preventing angiotensin II and AG1024-induced cell apoptosis, Leu27IGF2 appears to synergistically increase apoptosis in those cells. We further found cell apoptosis induction and an increase in the active form of caspase 3 in the treatment of cells with Leu27IGF2, but not IGF1. To detect the interaction between IGF2R and Gaq using the immunoprecipitation assay, we found that IGF2R could directly interact with Gaq and after treatment with Leu27IGF2 the binding ability of Gaq to IGF2R had increased. This sequentially resulted in the phosphorylation of phospholipase C-b, a key downstream modulator of Gaq, on serine 537. Moreover, disruption of the Gaq protein by small interferon RNA reduced the cell apoptosis induced by Leu27IGF2. Our findings demonstrate that IGF2R activation appears to induce cell apoptosis via Gaq-deriving signaling cascades and its effect is completely different from IGF1R survival signaling.