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David Brindley's research primarily focuses on understanding the changes in signal transduction that lead to increased growth of breast tumors, their metastasis, and the development of therapy resistance. He concentrates on the enzyme autotaxin (ATX), which is crucial for promoting wound healing. ATX produces lysophosphatidate (LPA), a compound activating G-protein coupled receptors. Studies show that activities of lipid phosphate phosphatases (LPPs), particularly LPP1 and LPP3, are decreased in breast tumors, suggesting a significant role of these enzymes in regulating tumor growth and metastasis. Furthermore, LPA signaling has been linked to inflammation in breast cancer, whereby tumors secrete inflammatory cytokines that stimulate ATX transcription and secretion from surrounding cells. Research indicates that inhibiting ATX activity can reduce over twenty inflammatory cytokines and chemokines, potentially decreasing tumor progression. Brindley's recent work includes examining the impact of cytomegalovirus (CMV) on breast cancer, providing insights into mechanisms of metastasis and the effects of viral infections on cancer therapy.
University of Alberta • Edmonton, AB
Professor in the Department of Biochemistry, focusing on breast cancer research.
Department: Mechanical Engineering and Engineering Management