Dissecting the multifaceted roles of autophagy in cancer initiation, growth, and metastasis: from molecular mechanisms to therapeutic applications.

Autophagy is a cytoplasmic defense mechanism that cells use to break and reprocess their intracellular components. This utilization of autophagy is regarded as a savior in nutrient-deficient and other stressful conditions. Hence, autophagy keeps contact with and responds to miscellaneous cellular tensions and diverse pathways of signal transductions, such as growth signaling and cellular death. Importantly, autophagy is regarded as an effective tumor suppressor because regular autophagic breakdown is essential for cellular maintenance and minimizing cellular damage. However, paradoxically, autophagy has also been observed to promote the events of malignancies. This review discussed the dual role of autophagy in cancer, emphasizing its influence on tumor survival and progression. Possessing such a dual contribution to the malignant establishment, the prevention of autophagy can potentially advocate for the advancement of malignant transformation. In contrast, for the context of the instituted tumor, the agents of preventing autophagy potently inhibit the advancement of the tumor. Key regulators, including calpain 1, mTORC1, and AMPK, modulate autophagy in response to nutritional conditions and stress. Oncogenic mutations like RAS and B-RAF underscore autophagy's pivotal role in cancer development. The review also delves into autophagy's context-dependent roles in tumorigenesis, metastasis, and the tumor microenvironment (TME). It also discusses the therapeutic effectiveness of autophagy for several cancers. The recent implication of autophagy in the control of both innate and antibody-mediated immune systems made it a center of attention to evaluating its role concerning tumor antigens and treatments of cancer.

Hyponatremia As A Marker Of Complicated Appendicitis.

Background: The most frequent cause of paediatric acute abdomen is acute appendicitis. If acute appendicitis is not treated promptly, one third of cases progress to complicated appendicitis. Complicated appendicitis is associated with significant morbidity and its management protocol differs significantly from that of uncomplicated appendicitis. In this study, we assessed the relationship between serum sodium levels and complicated appendicitis. Methods: We conducted a prospective observational study from July to December 2020 at the Department of Neonatal and Paediatric Surgery, The Children Hospital, Pakistan Institute of Medical Sciences, Islamabad, on a sample size of 140 patients who met inclusion and exclusion criteria. For this study, we divided the patients into two groups. Group 1 had uncomplicated appendicitis and Group 2 had complicated appendicitis. These findings were then compared to preoperative serum sodium (Na) levels. Results: The median serum sodium level in group 1 (uncomplicated appendicitis) was 137.81 mg/dl, while in group 2 it was 131.35 mg/dl (Complicated Appendicitis). The sensitivity and specificity of serum sodium levels at a cut-off point of less than 135 mg/dl were 84.80% and 89.40%, respectively. Conclusion: Hyponatremia is currently thought to be a new marker for differentiating between complicated and uncomplicated appendicitis. It is a low-cost, high efficiency predictive marker for diagnosing and differentiating complicated appendicitis in children.