Pancreatic cancer stem cells. J Clin Oncol 2008 Jun 10;26(17):2806-12
Date
06/10/2008Pubmed ID
18539958DOI
10.1200/JCO.2008.16.6702Scopus ID
2-s2.0-45549100014 (requires institutional sign-in at Scopus site) 327 CitationsAbstract
Cellular heterogeneity in cancer was observed decades ago by studies in mice which showed that distinct subpopulations of cells within a tumor mass are capable of driving tumorigenesis. Conceptualized from this finding was the stem-cell hypothesis for cancer, which suggests that only a specific subset of cancer cells within each tumor is responsible for tumor initiation and propagation, termed tumor initiating cells or cancer stem cells (CSCs). Recent data has been provided to support the existence of CSCs in human blood cell-derived cancers and solid organ tumors of the breast, brain, prostate, colon, and skin. Study of human pancreatic cancers has also revealed a specific subpopulation of cancer cells that possess the characteristics of CSCs. These pancreatic cancer stem cells express the cell surface markers CD44, CD24, and epithelial-specific antigen, and represent 0.5% to 1.0% of all pancreatic cancer cells. Along with the properties of self-renewal and multilineage differentiation, pancreatic CSCs display upregulation of important developmental genes that maintain self-renewal in normal stem cells, including Sonic hedgehog (SHH) and BMI-1. Signaling cascades that are integral in tumor metastasis are also upregulated in the pancreatic CSC. Understanding the biologic behavior and the molecular pathways that regulate growth, survival, and metastasis of pancreatic CSCs will help to identify novel therapeutic approaches to treat this dismal disease.
Author List
Lee CJ, Dosch J, Simeone DMMESH terms used to index this publication - Major topics in bold
AnimalsAntineoplastic Agents
Biomarkers, Tumor
Cell Differentiation
Cell Proliferation
Cell Separation
Drug Resistance, Neoplasm
Gene Expression Regulation, Neoplastic
Humans
Inflammation
Neoplasm Metastasis
Neoplastic Stem Cells
Pancreatic Neoplasms
Radiotherapy
Regeneration
Signal Transduction
Treatment Failure
