Researchers at Australia's Monash University have revealed the mechanism used by the most common form of adult leukemia to avoid detection by the immune system.

The discovery is a breakthrough in the search for a cure for chronic lymphocytic leukemia (CCL). This year, approximately 14,620 new cases of CCL will be diagnosed in the U.S. this year, and about 4,650 people will die from the disease.

CCL affects white blood cells in the body that normally fight infections in healthy people. Most people with CCL die of other diseases because their body doesn't produce the antibodies to fight infection.

Lead researcher Fabienne Mackay says that current treatments for leukemia kill all B cells — both cancerous and healthy — leaving patients even more vulnerable to infections than they were before treatment began.

"It turns out that cancer cells are very good at sabotaging the immune system, using various tricks that confuse immune cells and 'smoke screens' preventing immune cells from recognizing the cancer," said Mackay.

Mackay and her team of researchers figured out exactly how CCL confuses the immune system, and have found a way to stop it while protecting the patient's immune system.
Their discovery makes it possible to create treatments that will permit the body to fight the cancer naturally.

"The best weapon we have for fighting cancer is the immune system itself," says Mackay. "It can sense the presence of an infection but also the emergence of a cancer."

A protein called "B cell Activating Factor of the TNF Family" or BAFF allows B cells to survive. Each B cell has three different kinds of receptors — TACI, BAFF-R and BCMA — to detect the presence of BAFF in the blood.

But in leukemia patients, the TACI receptors of cancerous B cells produce too much of a protein called Interleukin-10 (IL-10), which tricks the immune system into thinking nothing is wrong with the body, allowing the cancer to thrive undetected.

"We found that when the receptor called TACI was blocked, it prevented the secretion of IL-10 without eliminating normal B cells," said Mackay.

"Without IL-10, the tumor can no longer keep the immune system at bay, which means the patient's immune system can be 'kick-started' again to fight infections and cancers.

"This is very exciting, because it means that the B cells stay alive and well to do their job in the immune system fighting other infections. It also means the over production of IL-10 is stopped, and the CCL tumor cells are now exposed to immune cells specialized in fighting cancers," she said.

Mackay believes her team's discoveries may apply to a number of types of cancer, and could revolutionize the way they are treated.