ical genomics research, ChemGenex recently initiated Phase I/II human clinical trials with Ceflatonin as a potential treatment for patients with acute promyelocytic leukemia (APL). Ceflatonin is a natural product compound with demonstrated clinical activity as a single agent in hematological malignancies and research suggests other therapeutic uses for Ceflatonin in lymphoma and as a chemopotentiator in solid tumors. The research reported by ChemGenex today demonstrates that Ceflatonin affects specific genes and cellular pathways both in vitro and in vivo, including genes known to play a role in leukemia and key cellular transcription factors that are up-regulated in many solid tumors.

Ceflatonin Effect on Gene Expression Studied both In Vitro and In Vivo

In the research presented today, the ChemGenex scientists used a high-density array system to analyze the effects of Ceflatonin on gene expression within a human colon cancer cell line in vitro and on tumor growth and gene expression in fibrosarcoma cells grown in mice.

The researchers reported both up- and down-regulation of a number of genes in vitro, including effects on genes from the histone family and transcription factor Jun. Histone proteins are an integral part of the structure of chromosomes, and modified forms of these proteins are understood to play a role in leukemia. Jun is an important transcription factor that is regulated in response to a variety of growth factors, and up-regulation of this gene is associated with many solid tumors. Studies of gene expression in response to Ceflatonin in vivo demonstrated up-regulation of a variety of genes with transportation function as well as some unknown genes.

Understanding the patterns of gene expression in response to Ceflatonin, both in vitro and in vivo, helps us to advance the development of this drug in multiple ways, said Anil Sehgal, Ph.D. director of molecular biology and genomics at ChemGenex. First, the patterns
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Contact: Joan Kureczka
JKureczka@aol.com
415-821-2413
Kureczka/Martin Associates
30-Oct-2001

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