As we get older, our bodies change in many ways—some visible, some hidden. One hidden change is something called clonal hematopoiesis (CH). This happens when blood stem cells in the bone marrow develop genetic mutations.
These cells then start making groups of blood cells that are genetically different from the rest. This condition itself isn’t cancer, but it can increase the risk of developing serious blood cancers later in life.
A new study led by Northwestern Medicine, and published in the Journal of Clinical Investigation, has found out why certain people with specific mutations—especially in a gene called TP53—are at much higher risk of progressing to leukemia, a type of blood cancer.
Dr. Yan Liu, an associate professor at Northwestern University and senior author of the study, explained that while many people with CH never develop cancer, those with TP53 mutations are much more likely to get leukemia. The research team wanted to understand what causes these mutated cells to grow and outnumber the healthy ones.
To find answers, the scientists studied mice that had the same kinds of mutations. They discovered that when the body is under inflammatory stress—such as from infections or other immune triggers—the mutated stem cells gain an advantage.
These mutated cells don’t respond to the inflammation like healthy cells do. Instead, they resist damage, while the healthy cells get weaker. This gives the mutated cells a chance to grow faster and take over.
The team also discovered that a part of the immune system called the NLRP1 inflammasome plays a big role in this process. This structure acts like an alarm system that reacts to danger in the body.
In people with TP53 mutations, this alarm goes off and causes more inflammation, which ironically helps the harmful cells thrive while hurting the healthy ones. It creates a cycle where inflammation keeps helping the bad cells grow.
As we age, the body’s level of chronic inflammation naturally increases. For people with TP53 mutations, this means that the risk of blood cancers grows even higher over time. The researchers also found that these mutations change how cells use RNA, which then keeps inflammation going in the bone marrow.
But there is hope. The study found that if you block one of the key inflammation signals—called IL-1B—the mutant cells lose their advantage. This finding could lead to new treatments that prevent blood cancers by stopping the inflammation before it causes too much harm.
Dr. Liu and his team believe this research could help doctors identify people who are at risk earlier and possibly stop leukemia before it begins. They are now looking at ways to test IL-1B-blocking treatments in people with TP53 or other similar mutations.
This study gives us a clearer picture of how aging, genetics, and inflammation can work together to raise cancer risks. It also opens the door to new strategies that could help people stay healthier as they age, especially those with known genetic risks.
If you care about cancer, please read studies that a low-carb diet could increase overall cancer risk, and vitamin D supplements could strongly reduce cancer death.
For more information about health, please see recent studies about how drinking milk affects the risks of heart disease and cancer and results showing higher intake of dairy foods linked to higher prostate cancer risk.
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