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Semin Cancer Biol. 2018 Sep 28. pii: S1044-579X(18)30116-0. doi: 10.1016/j.semcancer.2018.09.008. [Epub ahead of print]

Metabolism and epigenetics of pancreatic cancer stem cells.

Author information

1
Department of Surgery, University of Michigan, Ann Arbor, MI, United States.
2
Department of Surgery, University of Michigan, Ann Arbor, MI, United States; Rogel Cancer Center, University of Michigan, Ann Arbor, MI, United States.
3
Rogel Cancer Center, University of Michigan, Ann Arbor, MI, United States; Molecular and Integrative Physiology, University of Michigan Medical School, Ann Arbor, MI, United States.
4
Department of Surgery, University of Michigan, Ann Arbor, MI, United States; Rogel Cancer Center, University of Michigan, Ann Arbor, MI, United States. Electronic address: timofran@med.umich.edu.

Abstract

Pancreatic Cancer (PDA) is an aggressive malignancy characterized by early spread and a high mortality. Current studies suggest that a subpopulation of cells exist within tumors, cancer stem cell (CSC), which are capable of self-renewal and give rise to unique progeny which form the major neoplastic cellular component of tumors. While CSCs constitute a small cellular subpopulation within the tumor, their resistance to chemotherapy and radiation make them an important therapeutic target for eradication. Along with distinctive phenotypic properties, CSCs possess a unique metabolic plasticity allowing them to rapidly respond and adapt to environmental changes. These cells and their progeny also display a significantly altered epigenetic state with distinctive patterns of DNA methylation. Several mechanisms of cross-talk between epigenetic and metabolic pathways in PDA exist which ultimately contribute to the observed cellular plasticity and enhanced tumorigenesis. In this review we discuss various examples of this metabolic-epigenetic interplay and how it may constitute a new avenue for therapy specifically targeting CSCs in PDA.

KEYWORDS:

Acinar-ductal-metaplasia; Cancer stem cells; Epigenetics; Epithelial-to-mesenchymal transition; Metabolism; Pancreatic cancer; Stemness

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