Journal
CANCERS
Volume 11, Issue 8, Pages -Publisher
MDPI
DOI: 10.3390/cancers11081136
Keywords
cancer stem cells; pancreatic cancer; metastasis; EMT; stem cells
Categories
Funding
- German Cancer Aid (Max Eder Fellowship) [111746]
- German Cancer Aid Priority Program 'Translational Oncology [70112505]
- Hector Foundation Cancer Research grant [M65.1]
- Collaborative Research Centre grant of the German Research Foundation [316249678-SFB 1279]
- German Cancer Aid, Priority Program 'Translational Oncology [70112504]
- Ramon y Cajal Merit Award from the Ministerio de Economia y Competitividad, Spain [RYC-2012-12104]
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Metastasis and tumor progression are the major cause of death in patients suffering from pancreatic ductal adenocarcinoma. Tumor growth and especially dissemination are typically associated with activation of an epithelial-to-mesenchymal transition (EMT) program. This phenotypic transition from an epithelial to a mesenchymal state promotes migration and survival both during development and in cancer progression. When re-activated in pathological contexts such as cancer, this type of developmental process confers additional stemness properties to specific subsets of cells. Cancer stem cells (CSCs) are a subpopulation of cancer cells with stem-like features that are responsible for the propagation of the tumor as well as therapy resistance and cancer relapse, but also for circulating tumor cell release and metastasis. In support of this concept, EMT transcription factors generate cells with stem cell properties and mediate chemoresistance. However, their role in pancreatic ductal adenocarcinoma metastasis remains controversial. As such, a better characterization of CSC populations will be crucial in future development of therapies targeting these cells. In this review, we will discuss the latest updates on the mechanisms common to pancreas development and CSC-mediated tumor progression.
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