Finding and Killing the CRABs of Pancreatic Cancer Meredith E. Caldwell, David A. Tuveson  Gastroenterology  Volume 137, Issue 3, Pages 782-785 (September 2009) DOI: 10.1053/j.gastro.2009.07.035 Copyright © 2009 AGA Institute Terms and Conditions

Figure 1 CSCs/CRABs bridge the gap between tumor initiation and propagation. Cancer initiation requires bypass of intrinsic and extrinsic tumor-suppressive mechanisms, whereas cancer progression is dependent on effective turnover of cells and acquisition of increasingly malignant clones. In the pancreas, these fundamentally different processes are both potentially fuelled by CD133 positive CSCs/CRABs. It is likely CD133 positivity alone confers initiation capabilities whereas additional expression of CXCR4 enables invasive and metastatic behavior. Mueller et al demonstrate that both cell populations are effectively inhibited by a combination therapy of gemcitabine, cyclopamine, and rapamycin creating new possibilities for the treatment of pancreatic ductal adenocarcinoma. Gastroenterology 2009 137, 782-785DOI: (10.1053/j.gastro.2009.07.035) Copyright © 2009 AGA Institute Terms and Conditions