Open Access. Powered by Scholars. Published by Universities.®
- Keyword
-
- Adaptor Proteins (1)
- Adaptor Proteins, Signal Transducing (1)
- Alleles (1)
- Animals (1)
- Antioxidants (1)
-
- Cell Line (1)
- Cell Line, Tumor (1)
- Cell Proliferation (1)
- Cell Transformation (1)
- Cell Transformation, Neoplastic (1)
- Cells (1)
- Cells, Cultured (1)
- Cultured (1)
- Cytoskeletal Proteins (1)
- Extracellular Signal-Regulated MAP Kinases (1)
- Fibroblasts (1)
- Genes (1)
- Genes, myc (1)
- Humans (1)
- Intracellular Signaling Peptides and Proteins (1)
- JNK Mitogen-Activated Protein Kinases (1)
- MAP Kinase Signaling System (1)
- Mice (1)
- Mitogen-Activated Protein Kinase Kinases (1)
- Myc (1)
- NF-E2-Related Factor 2 (1)
- NIH 3T3 Cells (1)
- Neoplastic (1)
- Oncogenes (1)
- Oxidation-Reduction (1)
Articles 1 - 2 of 2
Full-Text Articles in Medicine and Health Sciences
Oncogene-Induced Nrf2 Transcription Promotes Ros Detoxification And Tumorigenesis., Gina M. Denicola, Florian A. Karreth, Timothy J. Humpton, Aarthi Gopinathan, Cong Wei, Kristopher Frese, Dipti Mangal, Kenneth H. Yu, Charles J. Yeo, Eric S. Calhoun, Francesca Scrimieri, Jordan M. Winter, Ralph H. Hruban, Christine Iacobuzio-Donahue, Scott E. Kern, Ian A Blair, David A. Tuveson
Oncogene-Induced Nrf2 Transcription Promotes Ros Detoxification And Tumorigenesis., Gina M. Denicola, Florian A. Karreth, Timothy J. Humpton, Aarthi Gopinathan, Cong Wei, Kristopher Frese, Dipti Mangal, Kenneth H. Yu, Charles J. Yeo, Eric S. Calhoun, Francesca Scrimieri, Jordan M. Winter, Ralph H. Hruban, Christine Iacobuzio-Donahue, Scott E. Kern, Ian A Blair, David A. Tuveson
Department of Surgery Faculty Papers
Reactive oxygen species (ROS) are mutagenic and may thereby promote cancer. Normally, ROS levels are tightly controlled by an inducible antioxidant program that responds to cellular stressors and is predominantly regulated by the transcription factor Nrf2 (also known as Nfe2l2) and its repressor protein Keap1 (refs 2-5). In contrast to the acute physiological regulation of Nrf2, in neoplasia there is evidence for increased basal activation of Nrf2. Indeed, somatic mutations that disrupt the Nrf2-Keap1 interaction to stabilize Nrf2 and increase the constitutive transcription of Nrf2 target genes were recently identified, indicating that enhanced ROS detoxification and additional Nrf2 functions may …
Serum Monocyte Chemoattractant Protein-1 In Pancreatic Cancer., Jennifer Sullivan, Qiaoke Gong, Terry Hyslop, Harish Lavu, Galina Chipitsyna, Charles Yeo, Hwyda A Arafat
Serum Monocyte Chemoattractant Protein-1 In Pancreatic Cancer., Jennifer Sullivan, Qiaoke Gong, Terry Hyslop, Harish Lavu, Galina Chipitsyna, Charles Yeo, Hwyda A Arafat
Department of Surgery Faculty Papers
Background/Aims. Pancreatic ductal adenocarcinoma (PDA) has etiological association with chronic inflammation. Elevated circulating levels of inflammatory mediators, such as monocyte chemoattractant protein-1 (MCP-1), are found in obese individuals. We hypothesized that serum MCP-1 levels are elevated in obese PDA patients. Methods. ELISA was used to analyze MCP-1 serum levels in PDA (n = 62) and intraductal papillary mucinous neoplasms (IPMN) (n = 27). Recursive partitioning statistical analysis investigated the relationship between log MCP-1 and clinicopathological parameters. Results. Log MCP-1 values were significantly (P < 0.05) elevated in patients with BMI ≥ 37.5. In patients with BMI < 37.5, average log MCP-1 values were significantly elevated in PDA patients when compared to IPMN patients. Within the IPMN group, higher log MCP-1 levels correlated with increased age. Recursive partitioning analysis of IPMN versus PDA revealed a strategy of predicting characteristics of patients who are more likely to have cancer. This strategy utilizes log MCP-1 as the primary factor and also utilizes smoking status, gender, and age. Conclusion. MCP-1 is a promising biomarker in pancreatic cancer. The potential of using MCP-1 to distinguish PDA from IPMN patients must be studied in larger populations to validate and demonstrate its eventual clinical utility.