Researchers at ETH Zurich have made a significant discovery in the fight against cancer metastasis, potentially paving the way for new treatments to prevent the spread of colorectal cancer to the liver.

In a study published today in Nature, a team led by Andreas Moor from the Department of Biosystems Science and Engineering at ETH Zurich’s Basel campus has identified key molecular mechanisms that allow colorectal cancer cells to colonize the liver.

“Nine times out of ten, metastasis is the cause of cancer deaths,” said Moor. “Despite significant advancements in treating primary tumors, medicine remains largely powerless against metastases.”

The researchers found that the interaction between specific proteins on the surface of liver cells and colorectal cancer cells plays a crucial role in the metastatic process. Liver cells with a protein called Plexin-B2 can interact with proteins from the semaphorin family on cancer cells, allowing the cancer cells to attach to the liver.

“Colorectal cancer cells with semaphorins on their surface are especially dangerous,” Moor said, citing clinical studies that show earlier and more frequent liver metastasis in tumors with high levels of semaphorin.

This interaction triggers fundamental changes in the cancer cells, allowing them to adapt to their new environment in the liver. The cancer cells undergo a process of “epithelisation,” forming structures similar to the folds found in intestines.

The discovery has implications beyond colorectal cancer. Further tests have shown that this mechanism also encourages metastasis in melanoma and pancreatic cancer.

While the path to potential treatments is still long, Moor is optimistic. “If we can inhibit the crucial interaction between plexin and semaphorin, it may be possible to prevent the cancer from establishing new tumors in the first place,” he said.

If efforts to inhibit the crucial interaction between plexin and semaphorin succeed, it may be possible to prevent the cancer from establishing new tumours in the first place. That’s because early on, when the relationships among the cells in this ecosystem have not yet been firmly established, tumour metastases are especially vulnerable, Moor explains.

He appears confident that an answer lies within this “critical period of time in the development of metastases”, even though the path to any potential treatment is still long.

(Inputs from ANI)