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Volume 15, Issue 3 (May 2013) 15, 323–327; 10.1038/aja.2013.40
Modelling synergistic interactions between HER2, Sprouty2 and PTEN in driving prostate carcinogenesis
Imran Ahmad1,2,3, Meiling Gao1, Rachana Patel1 and Hing Y Leung1,2,3
1 The Beatson Institute for Cancer Research, Glasgow G61 1BD, UK
2 Institute for Cancer Sciences, University of Glasgow, Glasgow G61 1BD, UK
3 Department of Urology, NHS Greater Glasgow and Clyde, Glasgow G12 0YN, UK
Correspondence: Professor HY Leung, (h.leung@beatson.gla.ac.uk)
Advance online publication 15 April 2013
| Abstract |
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Prostate cancer remains a major global health issue and a major cause of morbidity and mortality in men worldwide. Activation of androgen receptor and inactivation of the tumour suppressor gene phosphatase and tensin homologue (PTEN) represent two major events in prostate carcinogenesis. Using a range of clinical resources, in vitro and in vivo models, we explored potential complex interactions among receptor tyrosine kinases (such as HER2/3 and EGFR) and tumour suppressor genes, namely, Sprouty2 (SPRY2) and PTEN. The impacts on their downstream effectors (including PI3K and MAPK) to result in fine regulation of the signalling networks were also considered, which may represent important targets for developing treatment in the context of personalized medicine.
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