Scientists report on promising new approaches to induce cancer ce...( ther as a single agent or in combinatio...)

In the mouse studies, the researchers tested LY2181308 against survivin in xenograft tumor model using human melanoma cells implanted under the skin. Intravenous administration of the survivin antisense molecule LY2181308 to tumor-bearing nude mice significantly inhibited tumor growth compared to animals treated with saline or mis-match control oligonucleotide. Furthermore, they demonstrated that this anti-tumor activity was associated with significant inhibition of survivin expression in these xenograft tumors. Other studies are currently assessing the activity of LY2181308 and chemotherapeutic agents in the cancer model.

Killing cancer cells and endothelial cells with a VEGF-triggered cell death receptor: Abstract 407

Scientists today presented new research on inducing cancer cell suicide. Tumors stimulate new blood vessel growth in order to acquire oxygen and nutrients, a process called tumor angiogenesis, by secreting an angiogenic growth factor called VEGF. Researchers from the University of California, San Francisco today presented a novel treatment approach using the tumor's own weapon against itself by forcing VEGF to act as a cell death factor instead of a growth factor.

VEGF normally works by attaching to the extracellular region of VEGF receptor 2, which activates the intracellular region of the receptor to send growth signals. The research team created an artificial VEGF receptor, called R2Fas, in which the intracellular region of VEGF receptor 2 was replaced with a part of the Fas death receptor, which can trigger a process of cellular suicide termed apoptosis.

Blood vessel cells in culture normally grow when exposed to VEGF. When the R2Fas receptor was expressed in blood vessel cells, the cells were instead rapidly killed by VEGF, showing that VEGF acted as a death
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Contact: Warren Froelich
froelich@aacr.org
215-440-9300
American Association for Cancer Research
20-Nov-2003