Cancer becomes far more dangerous when it spreads, or metastasizes, from where it first starts to other parts of the body.
Doctors and scientists have been trying to understand why cancer spreads to certain organs, like the lungs or liver, more often than others. While many details are still unclear, a new study from Japan may finally offer some answers—along with a new way to possibly stop this deadly process.
The research was led by Professor Sachie Hiratsuka from Shinshu University School of Medicine and was published in the journal Nature Communications. The team focused on a protein in the blood called fibrinogen, which plays a key role in blood clotting. Their surprising finding? A tiny chemical change to this protein might help cancer cells find their way to the lungs.
This chemical change is known as citrullination. It happens when a building block of proteins, called arginine, is changed into another one called citrulline. The research team discovered that when fibrinogen goes through this change, it behaves differently.
It changes shape, its electrical charge changes, and it starts binding more easily to cancer cells. In simple terms, it turns into a sort of “welcome mat” for cancer, creating a soft landing spot in the lungs—what scientists call a “metastatic niche.”
But what causes this change in fibrinogen? The answer may lie in proteins called Serum Amyloid A (SAA). These are proteins made in the liver during times of stress or inflammation.
In earlier studies, Professor Hiratsuka’s team had noticed that fibrinogen often clumps in the lungs of mice and people with cancer, possibly helping cancer cells settle there. This time, they went further and discovered that SAAs actually trigger the citrullination process that turns fibrinogen into a tool for cancer spread.
To prove this idea, the team engineered mice to produce human versions of SAA proteins. These mice developed more lung tumors compared to regular mice, strongly supporting the idea that SAAs and citrullinated fibrinogen together play a key role in helping cancer spread to the lungs.
Even more promising is what came next. The researchers created a small piece of protein called CitFbg peptide, which acts like a blocker. It competes with citrullinated fibrinogen and prevents it from binding to cancer cells.
When this peptide was given to mice, it significantly reduced the number of lung tumors. The team even developed a special antibody that helps locate where citrullinated fibrinogen has built up in the lungs, allowing them to spot potential trouble zones early.
This discovery could lead to a new generation of cancer treatments that focus not just on killing cancer cells, but on stopping them from spreading in the first place. If doctors can identify places in the body where cancer is likely to spread, and block the signals that help it do so, they might prevent deadly metastasis before it even begins.
Of course, more research is needed. These results were found in mice, and clinical trials in humans will be needed to see if the same process happens in people—and if the new peptide treatment is safe and effective. But this is still a major breakthrough. It offers new hope in a field where treatments for late-stage cancer often fall short.
In the meantime, other studies have also shown that common anti-inflammatory drugs and even statins (cholesterol-lowering medications) might help in the fight against cancer by affecting how cells grow and spread. Some researchers are also studying natural compounds found in fruits and plants to see if they can slow cancer growth.
As science moves forward, studies like this one bring us closer to understanding—and eventually controlling—how and where cancer spreads. And that could save countless lives.
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