Cancer Cell 2017 07;32(1):3-5
Ludwig Institute for Cancer Research, New York, NY 10017, USA; The Wistar Institute, Philadelphia, PA 19104, USA. Electronic address:
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Cancer Cell 2017 07;32(1):71-87.e7
Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, NE 68198-5950, USA; Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE 68198, USA. Electronic address:
Poor response to cancer therapy due to resistance remains a clinical challenge. The present study establishes a widely prevalent mechanism of resistance to gemcitabine in pancreatic cancer, whereby increased glycolytic flux leads to glucose addiction in cancer cells and a corresponding increase in pyrimidine biosynthesis to enhance the intrinsic levels of deoxycytidine triphosphate (dCTP). Increased levels of dCTP diminish the effective levels of gemcitabine through molecular competition. Read More
Curr Cancer Drug Targets 2014 ;14(4):407-17
Department of Medical Oncology, First Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui, 233004, China.
Pancreatic cancer is one of the highly aggressive malignant diseases worldwide. To achieve better treatment outcome of pancreatic cancer, in the current study we explore the underlying molecular mechanism of drug resistance in pancreatic cancer cells. We found that resistance to gemcitabine is associated with epithelial-mesenchymal transition (EMT) phenotype in a panel of pancreatic cancer cell lines. Read More
BMC Cancer 2015 Feb 19;15:71. Epub 2015 Feb 19.
Department of Surgery, University Hospital Regensburg, University of Regensburg, Franz-Josef-Strauss Allee 11, 93053, Regensburg, Germany.
Background: Expression and activation of the cMET receptor have been implicated in tumor progression and resistance to chemotherapy in human pancreatic cancer. In this regard we assessed the effects of targeting cMET in pancreatic cancer models in vitro and in vivo.
Methods: Human (L3. Read More