Pamela L Rice
Affiliation: University of Colorado Health Sciences Center
- Sulindac metabolites induce caspase- and proteasome-dependent degradation of beta-catenin protein in human colon cancer cellsPamela L Rice
Department of Medicine, University of Colorado Health Sciences Center, Denver, CO 80262, USA
Mol Cancer Ther 2:885-92. 2003....
- Inhibition of extracellular-signal regulated kinases 1/2 is required for apoptosis of human colon cancer cells in vitro by sulindac metabolitesPamela L Rice
Veterans Administration Medical Center, Department of Medicine, University of Colorado Health Sciences Center, and University of Colorado Comprehensive Cancer Center, Denver, Colorado 80262, USA
Cancer Res 64:8148-51. 2004..These results suggest that inhibition of MEK/ERK signaling is necessary for the induction of apoptosis by sulindac metabolites...
- Sulindac independently modulates extracellular signal-regulated kinase 1/2 and cyclic GMP-dependent protein kinase signaling pathwaysPamela L Rice
Veterans Affairs Medical Center Denver, CO, USA
Mol Cancer Ther 5:746-54. 2006..Using similar combinatorial approaches in vivo may provide more effective, less toxic chemopreventive and chemotherapeutic strategies. Such therapies could dramatically reduce the incidence and death rate from colorectal cancer...
- Sulindac sulfide inhibits epidermal growth factor-induced phosphorylation of extracellular-regulated kinase 1/2 and Bad in human colon cancer cellsPamela L Rice
Division of Gastroenterology, Department of Medicine, University of Colorado Health Sciences Center, Denver, Colorado 80262, USA
Cancer Res 63:616-20. 2003..The ability of sulindac to block ERK1/2 signaling by the EGF receptor may account for at least part of its potent growth-inhibitory effects against cancer cells...
- Regulation of cytokine-induced prostanoid and nitric oxide synthesis by extracellular signal–regulated kinase 1/2 in lung epithelial cellsPamela L Rice
Veterans Affairs Medical Center, Denver, Colorado, USA
Exp Lung Res 36:558-71. 2010..Since tumor-derived cells were more sensitive than nontumorigenic cells to the antiproliferative effects of U0126, MEK1/2 inhibition may serve as an attractive chemotherapeutic target...
- Wound healing after trauma may predispose to lung cancer metastasis: review of potential mechanismsNicholas D Walter
Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Denver Anschutz Medical Campus, Denver, Colorado, USA
Am J Respir Cell Mol Biol 44:591-6. 2011..Further exploration of post-traumatic inflammatory oncotaxis may elucidate fundamental mechanisms of metastasis and could provide novel strategies to prevent cancer metastasis...