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Macroautophagy/autophagy is a highly conserved evolutionary mechanism involving lysosomes for the degradation of cytoplasmic components including organelles. The constitutive, basal level of autophagy is fundamental for preserving cellular homeostasis; however, alterations in autophagy can cause disease pathogenesis, including cancer. The role of autophagy in cancer is particularly complicated, since this process acts both as a tumor suppressor in precancerous stages but facilitates tumor progression during carcinogenesis and later stages of cancer progression. This shift between anti-tumor and pro-tumor roles may be influenced by genetic and environmental factors modulating key pathways such as those involving autophagy-related proteins, the PI3K-AKT-MTOR axis, and AMPK, which often show dysregulation in tumors. Autophagy regulates various cellular functions, including metabolism of glucose, glutamine, and lipids, cell proliferation, metastasis, and several types of cell death (apoptosis, ferroptosis, necroptosis and immunogenic cell death). These multifaceted roles demonstrate the potential of autophagy to affect DNA damage repair, cell death pathways, proliferation and survival, which are critical in determining cancer cells' response to chemotherapy. Therefore, targeting autophagy pathways presents a promising strategy to combat chemoresistance, as one of the major reasons for the failure in cancer patient treatment. Furthermore, autophagy modulates immune evasion and the function of immune cells such as T cells and dendritic cells, influencing the tumor microenvironment and cancer's biological behavior. However, the therapeutic targeting of autophagy is complex due to its dual role in promoting survival and inducing cell death in cancer cells, highlighting the need for strategies that consider both the beneficial and detrimental effects of autophagy modulation in cancer therapy. Hence, both inducers and inhibitors of autophagy have been introduced for the treatment of cancer. This review emphasizes the intricate interplay between autophagy, tumor biology, and immune responses, offering insights into potential therapeutic approaches that deploy autophagy in the cancer suppression. [ABSTRACT FROM AUTHOR]

• Novel investigation on the operative method of tethered spinal cord in children. • Strong advocate of real-time intraoperative neurophysiological monitoring during untethering process. • Proposition of some operative and nursing skills for the therapy of children with tethered spinal cord. To study the utility of neurophysiological monitoring in the micro-surgical treatments on children with Tethered Cord Syndrome (TCS). A total of 100 patients were included in this study. 51 children underwent micro-surgical treatments without neurophysiological monitoring (no monitoring group) from 2004 to 2009, whereas 49 children with neurophysiological monitoring (monitoring group) from 2010 to 2016. Postoperative evaluations demonstrated that more children in monitoring group (39, 80%) achieved total release than no monitoring group (36, 71%). Fewer new complications (9, 18%) were found in children of monitoring group than that of no monitoring group (19, 37%) (χ2 = 4.422, P < 0.05). Additionally, more children in monitoring group (34, 76%) achieved complete recovery or significant improvement than that of no monitoring group (24, 54%) (χ2 = 4.326, P < 0.05). This retrospective study provided the evidence supporting the hypothesis that intra-operative neurophysiological monitoring may better guide the surgical process, reduce the risk of post-operative complications, and improve the recovery of children with TCS. [ABSTRACT FROM AUTHOR]