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ScienceDaily (June 11, 2009) - University of Florida researchers have come up with a new gene therapy method to disrupt cancer growth by using a synthetic protein to induce blood clotting that cuts off a tumor's blood and nutrient supply. In mice implanted with human colorectal cancer cells, tumor volume decreased 53 percent and cancer cell growth slowed by 49 percent in those treated with a gene that encodes for the artificial protein, compared with those that were untreated.

A ground-breaking Canada-wide clinical trial led by Dr. Katherine Borden, at the Institute for Research in Immunology and Cancer (IRIC) of the Universit de Montral, has shown that a common anti-viral drug, ribavirin, can be beneficial in the treatment of cancer patients. Published in the journal Blood (First Edition), the study demonstrates that ribavirin suppresses the activities of the eIF4E gene in patients. This gene is dysregulated in 30 percent of cancers including breast, prostate, head and neck, colon and stomach cancer.

Glucose restriction can extend normal cell lifespan and impair precancerous cell growth through epigenetic control of hTERT and p16 expression. Li Y, Liu L, Tollefsbol TO. FASEB J. 2009 Dec 17. [Epub ahead of print] PMID: 20019239 doi: 10.1096/fj.09-149328 Cancer cells metabolize glucose at elevated rates and have a higher sensitivity to glucose reduction. However, the precise molecular mechanisms leading to different responses to glucose restriction between normal and cancer cells are not fully understood. We analyzed normal WI-38 and immortalized WI-38/S fetal lung fibroblasts and found that glucose restriction resulted in growth inhibition and apoptosis in WI-38/S cells, whereas it induced lifespan extension in WI-38 cells. Moreover, in WI-38/S cells glucose restriction decreased expression of hTERT (human telomerase reverse transcriptase) and increased expression of p16(INK4a). Opposite effects were found in the gene expression of hTERT and p16 in WI-38 cells in response to glucose restriction. The altered gene expression was partly due to glucose restriction-induced DNA methylation changes and chromatin remodeling of the hTERT and p16 promoters in normal and immortalized WI-38 cells. Furthermore, glucose restriction resulted in altered hTERT and p16 expression in response to epigenetic regulators in WI-38 rather than WI-38/S cells, suggesting that energy stress-induced differential epigenetic regulation may lead to different cellular fates in normal and precancerous cells. Collectively, these results provide new insights into the epigenetic mechanisms of a nutrient control strategy that may contribute to cancer therapy as well as antiaging approaches.

Targeted cancer therapy and gene therapy have been mentioned in the blue before, but oncolytic viruses are the hot young thing. For consideration in cancer treatment, an virus must replicate in and kill a high number of exclusively cancer cells, while sparing healthy tissue. A Philadelphia-based company called Neotropix has won awards for its research into a prime contender - the Seneca Valley Virus. It has been the subject of Phase I adult clinical trials, with Phase II adult and Phase I pediatric clinical trials to start this year. SVV has advantages over some other contenders in that it is a naturally occurring (lest we create a race of mutant zombies) organism and studies so far suggest it is not harmful to healthy human cells. While a number of other oncolytic viruses are being examined, NTX-010 seems able to treat a very wide range of common and rare forms of cancer, some of which are now considered uniformly fatal. In addition, unlike some other tested viruses, it can travel through the bloodstream to treat metastatic and not just local disease. Compared to the side-effects and late effects of chemotherapy and radiation treatment, and because many of the cancers ideal for treatment with an oncolytic virus have no surgical options, this may be the next big breakthrough.