Special Issue "Pathogenesis of Pancreatic Cancer"
Deadline for manuscript submissions: closed (30 November 2018).
Prof. Dr. Marco Falasca
Metabolic Signalling Group, School of Pharmacy and Biomedical Sciences | Faculty of Health Sciences. Curtin University, Perth, Australia
Website | E-Mail
Interests: signal transduction, cancer invasion and metastasis in prostate, breast and pancreatic cancers; phosphoinositide signalling; PI3-kinase/PDK1 signalling pathway
Pancreatic ductal adenocarcinoma (PDAC) is still one of the most aggressive and lethal malignancy in Western countries, with a low survival rate of around 5% that has remained unchanged for the last 40 years. The reason for this standstill resides in both the difficulty in diagnosing the disease at an early stage, due to non-specificity or lack of symptoms, and the inefficacy of the treatments currently available, caused by resistance to chemotherapy and radiotherapy. PDAC cells are characterised by a tendency to infiltrate into the endothelium basement membrane and neurons and to propagate speedily to distant organs through the lymphatic system, causing metastasis. At molecular level, it is known that the activation of oncogenes, such as KRAS and NOTCH, and the blocking of tumour suppressor genes like p16, p53, SMAD4 and PTEN, are involved in the initiation and advancement of this disease. In addition, various cell signalling pathways, such EGFR, Akt and NF-kB, have been found to be disrupted, contributing to PDAC evolution. Despite all these advances in the understanding of the molecular pathogenesis of PDAC, further insight in the knowledge of this disease and new efficacious therapeutic strategies are urgently required in order to improve the outcomes for PDAC patients.
Prof. Dr. Marco Falasca
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- pancreatic cancer
- pancreatic ductal adenocarcinoma
- molecular pathogenesis
- cancer biology