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Data presented at 93rd Annual Meeting of AACR
Press Release
SOURCE: SuperGen Inc.
Study Shows SuperGen's Decitabine Corrects DNA Methylation, Key Mechanism of Cancer Growth
DUBLIN, Calif., April 11 /PRNewswire-FirstCall/ -- SuperGen Inc. announced today the results of a clinical study demonstrating the company's anticancer drug decitabine's ability to alter the process of gene methylation, a crucial component in cancer growth. The data was presented at the 93rd Annual Meeting of the American Association of Cancer Research (AACR) in San Francisco.
Gene silencing by hypermethylation is rapidly being established as an early key event in the development of cancer. At the AACR Annual Meeting, more than 100 presentations and abstracts addressed hypermethylation, twice the number from last year. More than 15 studies used decitabine to reactivate silenced tumor suppressor genes.
The Phase I study, conducted at Huntsman's Cancer Institute in Salt Lake City, enrolled ten patients diagnosed with solid tumors who were given a 7-day continuous infusion of decitabine. Investigators reported that the drug was well tolerated and resulted in specific changes in gene promotor methylation.
"We are excited that scientists all over the world are studying decitabine," added Dr. Rubinfeld. "They have concluded that our drug is the most effective and selective agent available today to reactivate tumor suppressor genes by correcting the crucial methylation error.
"We are working closely with the National Cancer Institute (NCI) to develop decitabine in solid tumors under the terms of the Cooperative Research and Development Agreement, which we entered into in May 2000," said Dr. Rubinfeld. "The NCI has already completed two clinical studies and is initiating several others, including decitabine in combination of other agents, as a high priority, which we believe validates our belief in decitabine as a new important platform technology in the war against cancer."
Results from several preclinical studies have demonstrated that decitabine (5-aza-2-deoxy-cytidine) effectively demethylated and reactivated different tumor suppressor genes in cell-lines from breast cancer, mesothelioma, as well as lung, gastric and colorectal cancer.
Another study presented at AACR, conducted at the M.D. Anderson Cancer Center in Houston, showed hypermethylated tumor suppressor genes in 64 percent of tumor tissue taken from 90 patients with early stage non-small cell lung cancer. Hypermethylation of IGFBP3 (insulin-like growth factor binding protein-3) correlated with worse overall survival, concluded professor Wou K.I. Hong, president of the American Association of Cancer Research. Other studies showed that smoking was associated with early hypermethylation and silencing of the genes that are protective against cancer.