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Inhibiting Cxcr2 disrupts tumor-stromal interactions and improves survival http://www.ncbi.nlm.nih.gov/pubmed/21926469 Research out of Hal Moses, MD’s lab evaluated a mouse model of pancreatic cancer with an activating mutation of Kras and knockout of TGFb receptor type II (Tgfbr2). This mouse develops aggressive pancreatic cancer and appears dependent on Cxc family of chemokines. The researchers found that the Cxc chemokines induced connective tissue growth factor expression in the pancreatic stromal fibroblasts, not in the pancreatic ductal adenocarcinoma cells themselves. Treating the mice with a CXCR2 inhibitor blocked pancreatic cancer progression.

 This study was also written up in Genetic Engineering & Biotechnology News (http://www.genengnews.com/gen-news-highlights/scientists-say- blocking-chemokine-receptor-in-pancreatic-cancer-stromal-cells-helps-slow-cancer-/81245701/).

Nuclear receptor liver receptor homologue 1 (LRH-1) regulates pancreatic cancer cell growth http://www.ncbi.nlm.nih.gov/pubmed/21949357 This PNAS article discusses LRH-1, a regulator of gene transcription, and its newly discovered critical role in pancreatic cancer development and progression.

Zyflamend suppresses growth and sensitizes human pancreatic tumors to gemcitabine http://www.ncbi.nlm.nih.gov/pubmed/21935918 Kunnumakkara et al looked at Zyflamend, a polyherbal preparation with potent anti-inflammatory activities, and its role in sensitizing an orthotopic mouse pancreatic cancer model to treatment with gemcitabine. Their findings suggest that Zyflamend alone has inhibitory activity against pancreatic tumors, and further sensitizes the tumors to gemcitabine.

Toll-like receptor 9 agonist IMO cooperates with cetuximab in K-Ras mutant pancreatic cancer http://www.ncbi.nlm.nih.gov/pubmed/21890455 The authors investigated the combination of Toll-like receptor 9 agonist IMO with the anti-EGFR monoclonal antibody cetuximab in pancreatic and colorectal cancers in vitro and in vivo. Their data suggest that IMO markedly inhibits growth of K-Ras mutant colon and pancreatic cancers in vitro and in nude mice, and cooperates with cetuximab via multiple mechanisms of action.

Hedgehog signaling: Networking to nurture a promalignant tumor microenvironment http://www.ncbi.nlm.nih.gov/pubmed/21775419 This review published in Molecular Cancer Research focuses on the latest findings on the signaling pathways that are activated and/or regulated by molecules generated from Hedgehog signaling in cancer and cites promising clinical interventions, and discusses future directions.

<span style="font-family: Arial,Helvetica,sans-serif;"> Possible link between two type 2 diabetes drugs and pancreatic cancer, new research suggests http://www.sciencedaily.com/releases/2011/09/110917082746.htm

<span style="font-family: Arial,Helvetica,sans-serif; font-size: 11pt;">A Gastroenterology paper from July (http://www.ncbi.nlm.nih.gov/pubmed/21334333) picked up considerable media attention in September. Elashoff and colleagues at UCLA evaluated the FDA database of reported adverse events for those associated with glucagon-like peptide-1-based therapy against diabetes. The authors found a significant increase in pancreatitis in patients treated with these types of diabetes drugs, raising concern about subsequent increased risk of pancreatic cancer.


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