Pancreatic cancer cachexia is a complex, multifactorial syndrome characterized by progressive wasting of skeletal muscle and adipose tissue, contributing to poor prognosis and high mortality in pancreatic cancer patients. While muscle and fat loss are the hallmark features, pancreatic cancer cachexia is increasingly recognized as a systemic disorder involving extensive metabolic and inflammatory disruptions across multiple organs. Tumor-derived cachexia-inducing factors play a central role in driving systemic inflammation, metabolic dysregulation, and neuroendocrine abnormalities, leading to anorexia, gut dysbiosis, cardiac dysfunction, and pancreatic exocrine and endocrine insufficiency. These multi-organ disturbances form a vicious cycle that accelerates disease progression and complicates clinical management. In this review, we provide a comprehensive overview of pancreatic cancer cachexia, including its definitions, classification, and heterogeneous clinical presentations. We further examine recent findings on the molecular mediators of cachexia and their role in inter-organ communication networks. Additionally, we highlight advances in experimental models that enable the dissection of pancreatic cancer cachexia pathophysiology, and discuss emerging mechanism-based therapeutic strategies aimed at disrupting the cachexia cycle. A deeper understanding of the systemic nature of pancreatic cancer cachexia and the crosstalk among affected organs may inform the development of multi-targeted interventions and hold promise for improving patient outcomes.

Neuroendocrine neoplasms (NENs) are a group of malignancies arising from neuroendocrine cells and peptidergic neurons. The high heterogeneity of NENs leads to challenges and complexities in its diagnosis and treatment. Experts from relevant disciplines were convened by the Society of Neuroendocrine neoplasm of China Anti-Cancer Association to develop this first edition of the Chinese Guideline for diagnosis and treatment of NENs (2022) based on existing evidence combined with domestic and international guidelines and consensus. In this article, we summarize the important contents of this guideline and make further discussion on some controversial issues, with the aim to provide treatment reference in clinical practice.

Hyperlipidemic pancreatitis (HLP) is one of the most important causes of acute pancreatitis. The pathogenesis is associated with the accumulation of free fatty acids which can activate the inflammatory response. Compared with other causes, HLP is more likely to have the clinical features characterized by more severe symptoms, more complications, and higher likelihood of persistent organ failure. The HLP patients always need lipid lowering therapy such as apheresis or insulin therapy to reduce serum triglyceride rapidly. Assessment of the presence of hyperlipidemia in patients of acute pancreatitis and prompt management are crucial for the prognosis and the prevention of recurrence. This article reviews the etiology, pathogenesis, clinical features, and treatment of hypertriglyceridemia-induced acute pancreatitis.