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Conquer Cancer Health News

Scientists block key proteins to stall cancer's spread in mice


Cancer scientists working with mice have identified a way of blocking a chemical pathway that tumor cells use to spread to surrounding tissues and organs.

Researchers said closing the pathway like a biochemical border checkpoint offers a promising approach to managing the disease and limiting metastasis, or the circulation of cancer cells through the body.

So far, the pathway has been manipulated in experiments in mice only. The research was conducted by scientists at Columbia University and published in Thursday's issue of the journal Nature.

"This could lead to therapies that block the transition of a tumor from benign to malignant and keep local disease in check," said pathologist Lance Liotta of the National Cancer Institute in Bethesda, Maryland.

The experiments at Columbia focused on an important characteristic of tumor growth.

Both benign and malignant tumors grow in uncontrolled ways, but malignant cells invade surrounding tissue and distant organs. If those cells circulate throughout the body, they can spawn new and more vigorous tumors that defy treatment even after the original tumor has been surgically removed or killed by radiation and chemotherapy.

Researchers believe the malignant cells hijack the body's own chemical transport system.

The scientists found that the pathway uses two specific proteins: amphoterin and RAGE. RAGE is involved in many kinds of cell growth. Amphoterin is found on a type of fast-growing brain cell known as a neurite.

A team led by Anne Marie Schmidt at Columbia implanted cancerous tumors in mice. In experiments, they blocked the combined activity of the two proteins with specific combinations of antibodies. The tumors stopped growing and circulation of malignant cells dropped.

Schmidt said any potential cancer therapy based on the experiments probably would be used in combination with other treatments that cut off a tumor's blood supply and boost the patient's immune system.

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