Surgery (RMH) - Research Publications

Permanent URI for this collection

http://hdl.handle.net/11343/223

Filters

2016 - 2020 2
2
Reset filters

Settings
Statistics
Citations
Author: Ernst, Matthias × Author: Poh, Ashleigh × Author: Putoczki, Tracy ×

Search Results

Now showing 1 - 2 of 2
  • Item
    Thumbnail Image
    Mouse models for gastric cancer: Matching models to biological questions
    Poh, AR ; O'Donoghue, RJJ ; Ernst, M ; Putoczki, TL (WILEY, 2016-07)
    Gastric cancer is the third leading cause of cancer-related mortality worldwide. This is in part due to the asymptomatic nature of the disease, which often results in late-stage diagnosis, at which point there are limited treatment options. Even when treated successfully, gastric cancer patients have a high risk of tumor recurrence and acquired drug resistance. It is vital to gain a better understanding of the molecular mechanisms underlying gastric cancer pathogenesis to facilitate the design of new-targeted therapies that may improve patient survival. A number of chemically and genetically engineered mouse models of gastric cancer have provided significant insight into the contribution of genetic and environmental factors to disease onset and progression. This review outlines the strengths and limitations of current mouse models of gastric cancer and their relevance to the pre-clinical development of new therapeutics.
  • Item
    Thumbnail Image
    Loss of Bcl-G, a Bcl-2 family member, augments the development of inflammation-associated colorectal cancer
    Nguyen, PM ; Dagley, LF ; Preaudet, A ; Lam, N ; Giam, M ; Fung, KY ; Aizel, K ; van Duijneveldt, G ; Tan, CW ; Hirokawa, Y ; Yip, HYK ; Love, CG ; Poh, AR ; D' Cruz, A ; Burstroem, C ; Feltham, R ; Abdirahman, SM ; Meiselbach, K ; Low, RRJ ; Palmieri, M ; Ernst, M ; Webb, AI ; Burgess, T ; Sieber, OM ; Bouillet, P ; Putoczki, TL (NATURE PUBLISHING GROUP, 2020-02)
    Gastrointestinal epithelial cells provide a selective barrier that segregates the host immune system from luminal microorganisms, thereby contributing directly to the regulation of homeostasis. We have shown that from early embryonic development Bcl-G, a Bcl-2 protein family member with unknown function, was highly expressed in gastrointestinal epithelial cells. While Bcl-G was dispensable for normal growth and development in mice, the loss of Bcl-G resulted in accelerated progression of colitis-associated cancer. A label-free quantitative proteomics approach revealed that Bcl-G may contribute to the stability of a mucin network, which when disrupted, is linked to colon tumorigenesis. Consistent with this, we observed a significant reduction in Bcl-G expression in human colorectal tumors. Our study identifies an unappreciated role for Bcl-G in colon cancer.