Physiology
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Browsing Physiology by Author "Al-Dasooqi, N."
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Item Metadata only Chemotherapy-induced diarrhoea is associated with a modified microbiome in cancer patients(Wiley-Blackwell, 2009) Stringer, A.M.; Gibson, R.J.; Bowen, J.M.; Logan, R.M.; Al-Dasooqi, N.; Keefe, D.M.K.; Australia & New Zealand Medical & Surgical Gastrointestinal Week 2009 (21 Oct 2009 - 24 Oct 2009 : Sydney, N.S.W.)Item Metadata only Emerging evidence on the pathobiology of mucositis(Springer-Verlag, 2013) Al-Dasooqi, N.; Sonis, S.; Bowen, J.; Bateman, E.; Blijlevens, N.; Gibson, R.; Logan, R.; Nair, R.; Stringer, A.; Yazbeck, R.; Elad, S.; Lalla, R.BACKGROUND: Considerable progress has been made in our understanding of the biological basis for cancer therapy-induced mucosal barrier injury (mucositis). The last formal review of the subject by MASCC/ISOO was published in 2007; consequently, an update is timely. METHODS: Panel members reviewed the biomedical literature on mucositis pathobiology published between January 2005 and December 2011. RESULTS: Recent research has provided data on the contribution of tissue structure changes, inflammation and microbiome changes to the development of mucositis. Additional research has focused on targeted therapy-induced toxicity, toxicity clustering and the investigation of genetic polymorphisms in toxicity prediction. This review paper summarizes the recent evidence on these aspects of mucositis pathobiology. CONCLUSION: The ultimate goal of mucositis researchers is to identify the most appropriate targets for therapeutic interventions and to be able to predict toxicity risk and personalize interventions to genetically suitable patients. Continuing research efforts are needed to further our understanding of mucositis pathobiology and the pharmacogenomics of toxicity.Item Metadata only Gastrointestinal mucositis: the role of MMP-tight junction interactions in tissue injury(Springer Netherlands, 2014) Al-Dasooqi, N.; Wardill, H.; Gibson, R.Chemotherapy for cancer causes significant gut toxicity known as mucositis. The pathogenesis of mucositis is ill defined. Recent clinical research guidelines have highlighted epithelial junctional complexes as emerging targets within mucositis research. Given the robust biological evidence linking tight junctions and matrix metalloproteinases, key mediators of mucositis, tight junction proteins have received significant attention. Despite this, the link between tight junctions, matrix metalloproteinases and mucositis development is yet to be established. This critical review therefore aims to describe the role of matrix metalloproteinases in mucositis, and how matrix metalloproteinase-dependent tight junction disruption may contribute to the pathobiology of mucositis.