A team led by Associate Professor Jun-Ping Liu, from the Department of Immunology, has identified two proteins that are involved in stopping the gene from producing a protein called telomerase that is essential if cancer cells are to proliferate.

Telomerase plays a key role in controlling the life span of cells by modifying structures called telomeres that are found at the end of chromosomes.

Although it is involved in tumour development, telomerase is also found in modest quantities in most cells. It is plentiful in stem cells where it keeps the telomeres long, allowing the cells to keep dividing without limit which is necessary for the repair of damaged and worn out tissues throughout the human body.

However, studies have shown that telomerase also plays a key role in the formation of cancerous tumours. "It's the best indicator of cancer - 85 per cent better than any other tumour marker," Associate Professor Liu said. "What's more, telomerase is not associated with benign tumours; it's a marker for malignant tumours only.

"If we can control the production of telomerase we can prevent the immortality of cancer cells and therefore cancer formation."

Associate Professor Liu and his colleagues have been investigating breast cancer cells to identify the molecular signalling that is required to turn on, and also inhibit, the gene that produces telomerase. They have found two proteins Smad3 and c-Myc that are involved in turning off telomerase production. Their findings are published in the current issue of the Journal of Biological Chemistry.

"It's significant to find inhibitors of telomerase and we have found, for the first time, the pathway that inhibits telomerase in human cells," Associate Professor Liu said.

"This reveals an important mechanism for developing anti-cancer agents that mimic these proteins and thereby inhibit the production of telomerase. "

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Researchers were not able to stop the deterioration of insulin and its receptors. However, by administering PPAR, they were able to bypass the defects in insulin signaling and preserve the cells that need insulin to thrive. PPAR molecules go directly to the nucleus of cells and tell DNA to turn on or off genes that are normally regulated by insulin, thus preventing them from dying and allowing them to communicate with each other. The major effects of the PPAR treatments were to increase brain size, preserve insulin and IGF-II receptor bearing neurons, and preserve learning and memory.

"The trigger for dementia is the loss of insulin and IGF producing cells. The cells that need those growth factors subsequently die. This study shows you can block the second phase, which is responsible for dementia. This is great news for patients since you treat early stages of disease," de la Monte says.

Another promising result for Alzheimer's patients is that these drugs could be given in the form of a pill, de la Monte says. In the study, the drugs were injected to control the amounts administered.

"One of the most exciting findings was that peripheral (intraperitoneal) injection of the PPAR agonists either partially or completely rescued the brains from neurodegeneration," the authors write.

Alzheimer's appears to be caused by parallel abnormalities - impaired insulin signaling and oxidative stress, which is regulated by the genes NOS and NOX. The PPAR agonists treatments target both problems. They preserve the cells regulated by insulin and IGF, and they decrease oxidative stress, resulting in fewer lesions in the brain.

"If the diagnosis is suspected or patients are in the early phases of AD, there's a good possibility they could get treatment that will help them. It's possible that in the moderate phase, treatment will also help, but more work needs to be done to show that," de la Monte says.

Treatment is not likely to work in the late stages of the disease, she says, because the cells have already died.

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