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Cancers 2012, 4(4), 989-1035; doi:10.3390/cancers4040989
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Cancer Stem Cells, EMT, and Developmental Pathway Activation in Pancreatic Tumors

†,*  and *
Received: 10 September 2012; in revised form: 2 October 2012 / Accepted: 9 October 2012 / Published: 12 October 2012
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Abstract: Pancreatic cancer is a disease with remarkably poor patient survival rates. The frequent presence of metastases and profound chemoresistance pose a severe problem for the treatment of these tumors. Moreover, cross-talk between the tumor and the local micro-environment contributes to tumorigenicity, metastasis and chemoresistance. Compared to bulk tumor cells, cancer stem cells (CSC) have reduced sensitivity to chemotherapy. CSC are tumor cells with stem-like features that possess the ability to self-renew, but can also give rise to more differentiated progeny. CSC can be identified based on increased in vitro spheroid- or colony formation, enhanced in vivo tumor initiating potential, or expression of cell surface markers. Since CSC are thought to be required for the maintenance of a tumor cell population, these cells could possibly serve as a therapeutic target. There appears to be a causal relationship between CSC and epithelial-to-mesenchymal transition (EMT) in pancreatic tumors. The occurrence of EMT in pancreatic cancer cells is often accompanied by re-activation of developmental pathways, such as the Hedgehog, WNT, NOTCH, and Nodal/Activin pathways. Therapeutics based on CSC markers, EMT, developmental pathways, or tumor micro-environment could potentially be used to target pancreatic CSC. This may lead to a reduction of tumor growth, metastatic events, and chemoresistance in pancreatic cancer.
Keywords: pancreatic cancer; cancer stem cells; epithelial-to-mesenchymal transition; developmental pathways; tumor micro-environment; chemoresistance pancreatic cancer; cancer stem cells; epithelial-to-mesenchymal transition; developmental pathways; tumor micro-environment; chemoresistance
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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MDPI and ACS Style

Hindriksen, S.; Bijlsma, M.F. Cancer Stem Cells, EMT, and Developmental Pathway Activation in Pancreatic Tumors. Cancers 2012, 4, 989-1035.

AMA Style

Hindriksen S, Bijlsma MF. Cancer Stem Cells, EMT, and Developmental Pathway Activation in Pancreatic Tumors. Cancers. 2012; 4(4):989-1035.

Chicago/Turabian Style

Hindriksen, Sanne; Bijlsma, Maarten F. 2012. "Cancer Stem Cells, EMT, and Developmental Pathway Activation in Pancreatic Tumors." Cancers 4, no. 4: 989-1035.


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