The body’s cells can sense when they’re about to become cancerous, and they can alert the immune system when they’ve become so damaged that they should be removed from the body. Question is, would it be possible to fend off cancer altogether by capitalizing on this process and improving it to ensure all precancerous cells are flushed from the body before they can make trouble?
Scientists at the University of Edinburgh have discovered two key immune molecules that could make that possibility a reality. They’re called toll-like receptors (TLRs) 2 and 10 and they can detect when cancer-causing genes, or oncogenes, have become active. They published their observations in the journal Science Advances.
When oncogenes become active, they trigger a process called senescence, which prevents damaged cells from growing uncontrollably. But it's not a fool-proof process.
"Damaged cancer-causing cells become senescent and are then killed by the body's own immune system,” said Matthew Hoare, a scientist with Cancer Research UK Cambridge Institute, in a statement. “However, if the immune system does not destroy the senescent cell, the surrounding tissue can become inflamed, promoting cancer development.”
TLR2 and TLR10 are able to detect viruses and bacteria. By discovering their role in cancer detection, the University of Edinburgh scientists provided key insight into the molecular mechanisms that control senescence, which could lead to new strategies for fighting cancer, they believe.
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Finding new ways to control senescence is a popular pursuit in biotech, particularly as it pertains to aging. Last year, for example, Cleara Biotech pulled in seed funding after it showed in mice that its modified peptide drug could restore fitness, hair growth and kidney function in mouse models of aging. The drug was designed to selectively eliminate senescent cells. Unity Biotech raised $85 million in an IPO last year to pursue a similar strategy.
But targeting senescence as a way to treat age-related diseases, including cancer, has proven challenging. Wistar Institute scientists discovered that promoting senescence does slow down tumor growth, but it also boosts the production of inflammatory cytokines and chemokines that can actually help the cancer to survive. They are working on methods for inhibiting cytokine and chemokine genes.
The University of Edinburgh team believes interfering with TLR2/10 signaling could be a strategy for helping the body to clear pre-cancerous cells. The cells rely on the signals to become inflamed and set off on the road to becoming cancerous, making the two toll-like receptors ideal drug targets, they argued in the new study.