Jim scarlet
With a 5-year survival rate of only 3–5%, pancreatic ductal adenocarcinoma remains one of the most lethal solid tumours. A typical clinical presentation of an incurable disease is the result of its aggressive biology and resistance to conventional and targeted therapeutic agents once it is diagnosed. Desmoplasia, a dense stroma of fibroblasts and inflammatory cells, is the hallmark of the disease. It prevents oxygen from reaching the organ and creates a strong hypoxic environment within the tumor. We argue in this review that pancreatic cancer cells undergo oncogenic and metabolic changes, facilitating their proliferation, and that hypoxia is to blame for the tumour’s highly aggressive and metastatic characteristics. However, the molecular changes that cause pancreatic cancer cells to adapt their metabolism remain a mystery. Cachexia is a symptom of this illness that shows that it is a real metabolic disease. As a result, the development of this cancer must have involved metabolic pathways in this tumor that are probably intertwined in a complex interorgan dialogue. Pancreatic cancer cells would better be able to maintain their growth advantage and develop metastasis if fuel sources were restricted. Keywords Cachexia; Pancreatic cancer; Hypoxia; Metabolism
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