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	HEADLINES ARCHIVES MEDIA CENTER

May 2006 Issue

• International Collaboration Yields Promising Protein for Eye Infections
• New Target for Cancer Therapies
• Virus Turns Cancer Cannibalistic
• A Very Human Robot

International Collaboration Yields Promising Protein for Eye Infections

By Ilene Raymond
Editor-in-Chief
May 1, 2006

A protein found in various cell types, including the skin, has been discovered in the tissue covering the eye, according to a paper published in Cell Death and Differentiation by Mina Massaro-Giordano, M.D. of the University of Pennsylvania's Scheie Eye Institute and Marcella Macaluso, PhD. of the Sbarro Institute for Cancer Research and Molecular Medicine at Temple University. The protein, Plasminogen Activator Inhibitor Type 2 (PAI-2) may have future clinical implications in various pathologies of the ocular surface such as infection or dry eye.

In a paper presented at the Association for Research in Vision and Ophthalmology (ARVO) in Florida, the researchers showed that PAI-2 interacts with RB2/p130, a tumor suppressor gene in the nucleus of the epithelial cells in the cornea and conjunctiva of the eye. Their findings reveal that Interaction with RB2/p130 and chromatin modeling enzymes may affect how PAI-2 is expressed.

"There is a different expression of the protein between the epithelium of the cornea and conjunctiva cells," says Massaro-Giordano, lead researcher of the study and an assistant professor of ophthalmology, cataract and refractive surgery at Scheie. "This may help us understand the molecular mechanisms that dictate the different expression profiles of PAI-2 in human corneal and conjunctival epithelial cells."

The research was the result of collaboration between the Sbarro Institute for Cancer Research and Molecular Medicine and the University of Siena, Italy. Funds from SHRO and the National Institutes of Health supported the work.

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May 2006 Issue

New Target for Cancer Therapies

By Ilene Raymond
Editor-in-Chief
May 1, 2006

Interfering with a cell's cytoskeleton, the internal scaffolding that shapes the cell may kill cancer cells, slow tumor growth and boost a common chemotherapy drug, according to research appearing in the European Journal of Cancer.

Cancer involves rapid cell division and mobility of cancer cells, both dependent on the cytoskeleton. But until now the cytoskeleton has not been a target in treating cancer, according to Primal de Lanerolle, professor of physiology and biophysics at the University of Illinois at Chicago and principal author of the study.

The study found that ML-7, which inhibits an enzyme called myosin light chain kinases, could lead to apoptosis, or cell death, in cultured breast and prostate cancer cell lines.

When ML-7 was combined with etoposide, a chemotherapy drug used to treat solid tumors, the effectiveness of the drug was enhanced.

In animal models, ML-7 slowed growth of breast cancer and prostate cancer tumors. Furthermore when combined with etoposide, ML-7 cut tumor growth by 88.5 percent for breast cancer tumors and by 79.1 percent in prostate cancer tumors.

Like many chemotherapy drugs, etoposide has side effects.

"Reducing the dose of the drug without losing effectiveness would have important clinical benefits, "ML-7 seemed to be tolerated very well, without any overt toxic effects of its own."

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May 2006 Issue

Virus Turns Cancer Cannibalistic

By Ilene Raymond
Editor-in-Chief
May 1, 2006

It sounds like a horror film: a medically engineered adenovirus hunts down and infects deadly brain cancer, and then kills off tumor cells by forcing them to devour themselves. The process, called autophagy, has proved effective on malignant glioma cells in mice, producing enough self-cannibalism to shrink tumors and extend life spans according to senior author Seiji Kondo, M.D., PhD. Associate professor in the Department of Neurosurgery at M.D. Anderson in Houston, Texas.

How does it work? According to Kondo, the virus goes after telomerase, an enzyme present in 80 percent of brain tumors as a target. "Once the virus enters the cell, it needs telomerase to replicate. Since normal brain tissue lacks telomerase, the virus replicates only in diseased cells."

Researchers also decoded the mechanism of autophagy, a process in which cells consume part of themselves when nutrients are scarce or to recycle their components. A double membrane forms around the material to be eaten, and then everything is digested. HTERT-ad (human telomerase reverse transcriptase promoter regulated adenovirus) infected glioma cells and induced autophagy by inactivating a molecular pathway that ordinarily prevents cell self-cannibalization.

Results in mice showed that among those with malignant brain gliomas, those treated with three injections of hTERT-Ad lived an average of 53 days. Those on the control adenoviruses survived about 29 days. Two of the hTERT-Ad mice survived 60 days and had no detectable brain tumors.

In all cases, the dead cancer cells showed signs of autophagy - bits of virus and cavities with residual digested material. Cells did not die by apoptosis; a more better understood process of cell cancer death. Many current cancer therapies focus on restoring apoptosis - which systematically kills defective cells, a process suppressed in dysfunctional cancer cells.

Source: PMID: 16670388 [PubMed - in process]

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May 2006 Issue

A Very Human Robot

By Pierpaolo Basso
SHPress Editor
May 1, 2006

The Human Patient Simulator (HPS) - a computer-model-driven full-sized mannequin that mirrors human responses to a broad array of medical procedures -- recently helped train 400 Neapolitan doctors treat emergency heart conditions, the number one cause of death in Italy.

The HPS (also known as Stan for "Standard Man") blinks, breathes, and has a heartbeat and pulse. Doctors can practice everything from delivering intravenous drugs, intubations, ventilation, and catherization on the life like model.

The Neapolitan Medical Confederation, the Italian Minister of Health and the pharmaceutical company Pfizer organized the Italian training program.

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