INTRODUCTION: Testicular tumours in childhood have diverse characteristics for different age ranges. This study aimed to describe the pattern, presentation and outcomes of primary testicular tumours in a paediatric population. METHODS: A retrospective study was conducted from January 2010 to December 2020 on children (≤18 years) with a diagnosis of primary testicular tumour. Baseline demographics, clinical characteristics, pathology, treatment and outcomes of these patients were analysed. The data were entered into IBM SPSS Statistics version 20.0. Chi-square test and Fisher's exact test were applied to find the statistical significance, which was set at P value ≤ 0.05. RESULTS: The study included 115 males, with 85 (73.9%) patients in the prepubertal age range with a mean age of 2.53 ± 2.06 years and 30 (26.1%) patients in the postpubertal group with a mean age of 15.73 ± 1.25 years. Yolk sac tumour was the most common (62.6%) histological subtype. Majority (46.1%) of patients had stage I disease on presentation, while 29.6% had stage IV disease. All patients underwent upfront high inguinal radical orchiectomy, which was followed by platinum-based adjuvant chemotherapy in 67% of the patients. The five-year event-free survival and overall survival for all patients were 75% and 91%, respectively. CONCLUSION Primary testicular tumours follow a bimodal age distribution pattern. Majority of patients can be cured with platinum-based chemotherapy despite having advanced disease at presentation.
Humans ; Male ; Testicular Neoplasms/mortality* ; Retrospective Studies ; Adolescent ; Child ; Child, Preschool ; Orchiectomy/methods* ; Chemotherapy, Adjuvant ; Treatment Outcome ; Neoplasm Staging ; Infant ; Endodermal Sinus Tumor/therapy* ; Neoplasms, Germ Cell and Embryonal

Flavonoids have an ability to suppress various ion channels. We determined whether one of flavonoids, cyanidin-3-glucoside, affects adenosine 5'-triphosphate (ATP)-induced calcium signaling using digital imaging methods for intracellular free Ca2+ concentration ([Ca2+]i), reactive oxygen species (ROS) and mitochondrial membrane potential in PC12 cells. Treatment with ATP (100microM) for 90 sec induced [Ca2+]i increases in PC12 cells. Pretreatment with cyanidin-3-glucoside (1micro g/ml to 100microg/ml) for 30 min inhibited the ATP-induced [Ca2+]i increases in a concentration-dependent manner (IC50=15.3microg/ml). Pretreatment with cyanidin-3-glucoside (15microg/ml) for 30 min significantly inhibited the ATP-induced [Ca2+]i responses following removal of extracellular Ca2+ or depletion of intracellular [Ca2+]i stores. Cyanidin-3-glucoside also significantly inhibited the relatively specific P2X2 receptor agonist 2-MeSATP-induced [Ca2+]i responses. Cyanidin-3-glucoside significantly inhibited the thapsigargin or ATP-induced store-operated calcium entry. Cyanidin-3-glucoside significantly inhibited the ATP-induced [Ca2+]i responses in the presence of nimodipine and omega-conotoxin. Cyanidin-3-glucoside also significantly inhibited KCl (50 mM)-induced [Ca2+]i increases. Cyanidin-3-glucoside significantly inhibited ATP-induced mitochondrial depolarization. The intracellular Ca2+ chelator BAPTA-AM or the mitochondrial Ca2+ uniporter inhibitor RU360 blocked the ATP-induced mitochondrial depolarization in the presence of cyanidin-3-glucoside. Cyanidin-3-glucoside blocked ATP-induced formation of ROS. BAPTA-AM further decreased the formation of ROS in the presence of cyanidin-3-glucoside. All these results suggest that cyanidin-3-glucoside inhibits ATP-induced calcium signaling in PC12 cells by inhibiting multiple pathways which are the influx of extracellular Ca2+ through the nimodipine and omega-conotoxin-sensitive and -insensitive pathways and the release of Ca2+ from intracellular stores. In addition, cyanidin-3-glucoside inhibits ATP-induced formation of ROS by inhibiting Ca2+-induced mitochondrial depolarization.
Adenosine ; Adenosine Triphosphate ; Animals ; Calcium ; Calcium Signaling ; Flavonoids ; Ion Channels ; Ion Transport ; Membrane Potential, Mitochondrial ; Nimodipine ; omega-Conotoxins ; PC12 Cells* ; Reactive Oxygen Species ; Receptors, Purinergic P2X2 ; Thapsigargin