Cambridge scientists have discovered how cancer spreads

Cambridge scientists have discovered how cancer spreads

Metastasis, the disease’s deadliest and best-known hallmark, gives cancer the ability to spread throughout the body, often overwhelming immune defenses and even the best treatments.

Although it is the primary cause of cancer death, we still don’t know much about metastasis. But now scientists at the Cambridge Institute of Cancer Research UK (CRUK) at the University of Cambridge have discovered the mechanism behind metastasis.

“The development of anti-metastatic therapies has proven difficult because it has proven difficult to find targets in primary tumors that drive metastasis,” says Eric Rahrmann, a postdoctoral fellow in the lab of study leader Richard Gilbertson, Freethink.

The chameleon’s abilities and protective microenvironment—a shield around them that helps tumors grow and prevents the body from fighting back—helped keep the mechanisms of metastasis elusive, Rahrmann says.

Metastasis gives cancer the ability to spread throughout the body, often overwhelming immune defenses and even the best treatments.

New research, published in Nature Genetics, has identified a protein cell structure called NALCN (“sodium leak channel, non-selective”) as a “key regulator” of metastasis. These channels are found on cell membranes and control the flow of sodium into and out of the cell.

Removing or blocking NALCN activity in mice with cancer “significantly increased the number of circulating tumor cells (CTCs) and metastases,” the authors wrote in their paper.

The study also turns on its head the common understanding of metastasis – that it’s just a cancer trick – showing that healthy cells can and do jump between organs too.

When NALCN was blocked in mice that never developed cancer, the researchers found that healthy cells were also released and circulated throughout the body.

They observed how healthy pancreatic cells migrated to the kidney and then became healthy kidney cells, New Atlas reported.

“Our models showed that even in the absence of a tumor, loss of NALCN function leads to increased release of apparently normal epithelial stem-like cells into the bloodstream,” says Rahrmann.

Researchers have found a mechanism for metastasis that we may be able to use to repair damaged organs in the future.

“These findings are among the most important to come out of my lab in three decades,” Gilbertson said.

“Not only have we identified one of the elusive drivers of metastasis, but we have also turned conventional understanding of the problem on its head and shown how cancer hijacks processes in healthy cells for its own gains.”

If confirmed by further research, the discovery could provide a target for stopping or slowing metastasis – as well as opening the door to using our own cells to repair damaged organs.

“Further investigation of this process may lead to a better understanding of how to use our intrinsic epithelial stem cells, which reside in many of our organs, to be mobilized throughout the body to repair ourselves,” says Rahrmann.

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