Pancreatic cancer: Pathogenesis, prevention and treatment

Abstract

Pancreatic cancer is the fourth leading cause of cancer death in the United States with a very low survival rate of 5 years. To better design new preventive and/or therapeutic strategies for the fight against pancreatic cancer, the knowledge of the pathogenesis of pancreatic cancer at the molecular level is very important. It has been known that the development and the progression of pancreatic cancer are caused by the activation of oncogenes, the inactivation of tumor suppressor genes, and the deregulation of many signaling pathways among which the EGFR, Akt, and NF-κB pathways appear to be most relevant. Therefore, the strategies targeting EGFR, Akt, NF-κB, and their downstream signaling could be promising for the prevention and/or treatment of pancreatic cancer. In this brief review, we will summarize the current knowledge regarding the pathogenesis, prevention, and treatment of pancreatic cancer.

Curcumin inhibits hypoxia-induced epithelial-mesenchymal transition in pancreatic cancer cells via suppression of the hedgehog signaling pathway

“…In 2015, it was estimated that 48,960 subjects will be newly diagnosed with pancreatic cancer and will account for 40,560 cancer-related deaths in the United States (1). Surgical resection remains the only way to cure this severe disease, however, due to the high metastatic rate, the majority of patients are diagnosed at an advanced inoperable stage, and less than 20% of patients are amenable for surgery (2). Even those patients with seemingly resectable pancreatic tumor are not always cured by surgery due to the microscopic systemic spread of cancer cells before the operation intervention (3).…”

Co-expression of FOXL1 and PP2A inhibits proliferation inducing apoptosis in pancreatic cancer cells via promoting TRAIL and reducing phosphorylated MYC

“…The pathogenesis and the incurable nature of pancreatic cancer, and the rapid metastasis and the poor response to chemo-drugs might contribute to the poor prognosis (1,36). Several pathways have been recognized to regulate the pathogenesis or progression of pancreatic cancers.…”

Pankreas Duktal Adenokarsinomuna Yaklaşımda NF-Kappa B’nin Rolü

“…Tümör supresör genler, mutasyon, delesyon veya hipermetilasyon ile aktive edilebilir. Özellikle p16, p53, SMAD4, PTEN, pankreas kanserinde hedef genlerdir 54 . P53, apoptotik hücre ölümününün indüksiyonunda önemli bir role sahiptir.…”

“…Karsinogenez sırasında p53 inaktivasyonu kontrolsüz hücre büyümesine ve hücre yaşam süresinin uzamasına neden olur. Ayrıca p53 genindeki değişiklikler K-ras mutasyonu ile ilişkilidir 54 . Pankreas kanser patogenezinde ortak aktiviteleri önemli bir yer almaktadır.…”