35IN - Pancreatic cancer

Date 29 September 2014
Event ESMO 2014
Session Towards personalised medicine in gastric, pancreatic and liver cancer: From “omics” research to treatment
Topics Pancreatic Cancer
Presenter Manuel Hidalgo
Citation Annals of Oncology (2014) 25 (suppl_4): iv14-iv14. 10.1093/annonc/mdu297
Authors M. Hidalgo
  • Ciocc, Centro Integral Oncologico Clara Campal, ES-28029 - Madrid/ES

Abstract

Body

Abstract:

Ductal adenocarcinoma of the pancreas (PDAC), also known as pancreatic cancer, is the fourth cause of cancer related deaths in western countries. While some patients develop PDAC in the context of hereditary cancer syndromes, the vast majority of cases are sporadic with only tobacco used consistently associated with a higher risk. Most patients present or develop metastatic disease during their illness. After more than 20 years of negative clinical trials, two recent randomize trials have demonstrated an improvement in survival. While clinical progress has been limited, our understanding of the molecular and cellular biology of PDAC has advanced substantially recently. From a genomic perspective, PDAC is a highly complex, heterogeneous and unstable disease. Unfortunately, the most common mutated genes such as KRAS, p53, p16 and SMAD4 are not drug targets currently. Preclinical studies, however, are staring to provide clues as to how to attack these mutations. One of the hallmarks of PDAC is the high desmoplastic reaction that accompanies the disease. Recent studies have paid attention to the PDAC stroma as a strategic therapeutic compartment. Indeed, preclinical and clinical studies suggest that one of the mechanisms of action of Nab-paclitaxel, the most recently approved agent in PDAC may indeed be disruption of the cancer stroma. A series of novel agents are been developed to target the stroma. Finally, several groups have identified a subset of cancer stem cells in PDAC. These low frequency cells are considered to be chemo and radioresistant and responsible for cancer recurrence after treatment failure. There is significant interest in developing new agents against targeting CSC pathways and this will be reviewed.

Disclosure:

The author has declared no conflicts of interest.