All treatments for cancer are based on the concept of exploiting the difference between cancerous and normal cells. Chronic hypoxia—severely reduced oxygen flow to tissues—is a hallmark of many tumors, and causes changes in gene expression within tissues. One such gene, the transcription activator hypoxia-inducible factor 1 (HIF-1), is expressed in cells that lack oxygen and has become the object of cancer research because of its role in stimulating the expression of other genes that enable a cell to survive in hypoxic conditions.
Based on the idea that stopping the action of HIF-1 in cancerous cells would prevent their survival, David Livingston and colleagues at Harvard Medical School produced a polypeptide that interferes with the regulation of HIF-1 and its subsequent actions on other genes (Nature Medicine, Vol. 6, Issue 12, 01 Dec 2000). They show that the polypeptide is able to slow tumor growth in cells. Peter Ratcliffe and colleagues from the Henry Wellcome Building of Genomic Medicine in the UK, discuss the clinical feasibility of the strategy as an anticancer treatment in a News & Views article. CONTACT: Dr David M Livingston The Dana-Farber Cancer Institute Harvard Medical School 44 Binney Street Boston, Massachusetts 02115 USA Tel:+1 617 632 3074 Email: david_livingston@dfci.harvard.edu Dr Peter Ratcliffe Professor of Medicine Wellcome Trust Centre for Human Genetics Oxford OX3 7BN Tel: +44 1865 287531 Email: peter.ratcliffe@molecular-medicine.oxford.ac.uk (C) Nature Medicine press release.
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