Stop cancer before it develops

The body's cells can smell when they are about to become cancerous and they can alert the immune system when they are so badly damaged that they should be removed from the body. The question is: would it be possible to fight cancer by capitalizing on this process and improving it so that all precancerous cells are removed from the body before causing problems?

Scientists from the University of Edinburgh have discovered two key immune molecules that could concretize this possibility. They are called toll receivers (TLRs) 2 and 10 and can detect when carcinogenic 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 the uncontrollable growth of damaged cells. But it is not an infallible process.

"The damaged cancer cells become senescent and are then killed by the body's immune system," said Matthew Hoare, a scientist at Cancer Research UK's Cambridge Institute, in a statement. "However, if the immune system does not destroy the senescent cell, the surrounding tissue can become inflamed, promoting the development of cancer."

TLR2 and TLR10 are able to detect viruses and bacteria. By discovering their role in cancer detection, scientists at the University of Edinburgh have provided vital insights into the molecular mechanisms that control senescence, which could lead to new strategies for fighting cancer , they say.

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The search for new ways to control senescence is a popular activity in biotechnology, particularly with regard to aging. Last year, for example, Cleara Biotech obtained seed funding after showing mice that its modified peptide drug could restore fitness, hair growth and kidney function in aging mouse models. The drug has been designed to selectively remove senescent cells. Unity Biotech raised $ 85 million in an IPO last year to pursue a similar strategy.

But targeting senescence as a means of treating age-related diseases, including cancer, has proven difficult. Scientists at the Wistar Institute have discovered that promoting senescence slows down tumor growth, but also stimulates the production of inflammatory cytokines and chemokines that can actually help cancer survive. They are working on methods of inhibiting the genes of cytokines and chemokines.

The team at the University of Edinburgh believes that TLR2 / 10 signaling interference may be a strategy to help the body eliminate precancerous cells. The cells rely on the signals to ignite and get on their way to becoming cancerous, making both ideal receptors ideal drug targets, they explained in the new study.