Published online Aug 21, 2014. doi: 10.3748/wjg.v20.i31.10790
Revised: February 7, 2014
Accepted: April 5, 2014
Published online: August 21, 2014
Pancreatic cancer is one of the most aggressive and lethal malignancies. Despite remarkable progress in understanding pancreatic carcinogenesis at the molecular level, as well as progress in new therapeutic approaches, pancreatic cancer remains a disease with a dismal prognosis. Among the mechanisms responsible for drug resistance, the most relevant are changes in individual genes or signaling pathways and the presence of highly resistant cancer stem cells (CSCs). In pancreatic cancer, CSCs represent 0.2%-0.8% of pancreatic cancer cells and are considered to be responsible for tumor growth, invasion, metastasis and recurrence. CSCs have been extensively studied as of late to identify specific surface markers to ensure reliable sorting and for signaling pathways identified to play a pivotal role in CSC self-renewal. Involvement of CSCs in pancreatic cancer pathogenesis has also highlighted these cells as the preferential targets for therapy. The present review is an update of the results in two main fields of research in pancreatic cancer, pathogenesis and therapy, focused on the narrow perspective of CSCs.
Core tip: Pancreatic cancer is one of the most aggressive and lethal malignancies, despite remarkable progress in understanding pancreatic carcinogenesis and new therapeutic approaches. The presence of highly resistant cancer stem cells (CSCs) and the changes in their signaling pathways lead to drug resistance in pancreatic cancer. CSCs are considered responsible for tumor growth, invasion, metastasis and recurrence. CSC involvement in pancreatic cancer pathogenesis has also highlighted them as preferential targets for therapy. This review is an update of the results in two main fields of research in pancreatic cancer, pathogenesis and therapy, focused on the narrow perspective of CSCs.