Pancreatic ductal adenocarcinoma (PDAC), one of the most aggressive solid malignancies, is characterized by the presence of oncogenic KRAS mutations, poor response to current therapies, prone to metastasis, and a low 5-year overall survival rate. Macroautophagy (herein referred to as autophagy) is a lysosome-dependent degradation system that forms a series of dynamic membrane structures to engulf, degrade, and recycle various cargoes, such as unused proteins, damaged organelles, and invading pathogens. Autophagy is usually upregulated in established cancers, but it plays a dual role in the regulation of the initiation and progression of PDAC. As a type of selective autophagy, mitophagy is a mitochondrial quality control mechanism that uses ubiquitin-dependent (e.g., the PINK1-PRKN pathway) and -independent (e.g., BNIP3L/NIX, FUNDC1, and BNIP3) pathways to regulate mitochondrial turnover and participate in the modulation of metabolism and cell death. Genetically engineered mouse models indicate that the loss of PINK1 or PRKN promotes, whereas the depletion of BNIP3L inhibits oncogenic KRAS-driven pancreatic tumorigenesis. Mitophagy also play a dual role in the regulation of the anticancer activity of certain cytotoxic agents (e.g., rocaglamide A, dichloroacetate, fisetin, and P. suffruticosa extracts) in PDAC cells or xenograft models. In this min-review, we summarize the latest advances in understanding the complex role of mitophagy in the occurrence and treatment of PDAC. Pancreatic cancer begins in the tissues of your pancreas — an organ in your abdomen that lies behind the lower part of your stomach. Your pancreas releases enzymes that aid digestion and produces hormones that help manage your blood sugar. Several types of growths can occur in the pancreas, including cancerous and noncancerous tumors. The most common type of cancer that forms in the pancreas begins in the cells that line the ducts that carry digestive enzymes out of the pancreas (pancreatic ductal adenocarcinoma). Pancreatic cancer is seldom detected at its early stages when it's most curable. This is because it often doesn't cause symptoms until after it has spread to other organs. Pancreatic cancer treatment options are chosen based on the extent of the cancer. Options may include surgery, chemotherapy, radiation therapy or a combination of these.

European Journal of Clinical Oncology Cancer poses a major challenge to development; it undermines socio-economic advances throughout the world. It is estimated that the number of patients with cancer would increase from 12.7 million in the year 2008 to 22.2 million by 2030. It is universally agreed that the condition is reaching epidemic proportions. At this time, the European Journal of Clinical Oncology is conveniently placed in the scholarly communication milieu to help counter the menace of cancer by aiding the development of novel treatment strategies, by providing novel insights into the mechanisms underlying this complex disease.

European Journal of Clinical Oncology publishes peer-reviewed original research articles, review articles, short communications, expert opinions, commentaries and letters/editorials based on open access policy. Author(s) are invited to submit their manuscripts as an e-mail attachment for fast and efficient processing. Aims & scope of the journal, key words, indexing as well as bibliographic information can be accessed at https://www.iomcworld.org/european-clinical-oncology.html

John Robert

Managing Editor
European Journal of Clinical Oncology
Mail ID: oncology@scholarlymed.com