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Most human tumours harbour genetic mutations in key tumour suppressor genes of the p53 pathway, but cancers of the retina were, until now, thought the exception to the rule. In the 02 November 2006 issue of Nature (Vol. 444, No. 7115, pp 61-66), researchers provide evidence implicating inactivation of the tumour suppressor gene p53 in retinoblastoma, and suggest a revised chemotherapy protocol that they hope will minimize side effects and maximize cancer cell death.
Retinoblastomas, which are caused by mutations in the RB1 gene, affect mainly children. Michael A. Dyer and colleagues show that amplification of a gene called MDMX can inactivate the p53 pathway and contribute to the development of these cancers. They suggest treating patients with two drugs, topotecan and nutlin-3, simultaneously. Topotecan is a standard chemotherapy drug, and nutlin-3 is a small-molecule inhibitor which binds to MDMX and blocks its interaction with p53. The combination kills retinoblastoma cells in culture and reduces tumour burden by more than 80-fold when human retinoblastoma cells are transplanted into rat eyes. CONTACT Michael A. Dyer (St. Jude Children's Research Hospital, Memphis, TN, USA)
E-mail: michael.dyer@stjude.org Valerie Wallace (Ottawa Hospital Research Institute, Canada)
E-mail: vwallace@ohri.ca (C) Nature press release.
Message posted by: Trevor M. D'Souza
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