A drug often used to treat asthma and allergies may also help fight aggressive cancers, according to new US research.
The study revealed how tumors hijack common white blood cells to evade immunotherapy.
Scientists say their findings in mice and human tissues point to a new way to improve treatment for tough tumors—like triple-negative breast cancer—on which immunotherapy often fails.
The best news is the breakthrough could quickly move into clinical testing because the drug—montelukast, commonly known by the brand name Singulair—is already approved by the US Food and Drug Administration.
The research team from Northwestern University in Illinois explained that at the center of the discovery is a molecule called CysLTR1, which is best known for its role in asthma and inflammation.
Drugs that block it, such as montelukast, have been prescribed for decades to treat asthma.
The Northwestern team learned that many cancers exploit CysLTR1 to resist treatment. Specifically, the tumors trick the immune system into helping them grow by increasing a group of white blood cells called neutrophils.
They discovered it’s controlled by the CysLTR1 molecule, which acts as an on/off switch.
“When we turned off this switch, either genetically or with existing drugs, we not only slowed tumor growth, but also helped the immune system recover its ability to fight the cancer,” said study senior author Professor Bin Zhang.
MORE GOOD CANCER NEWS:
• Groundbreaking Bowel Cancer Trial Had Zero Relapses for Patients After 33 Months
• Prostate Cancer Patients Offered Fresh Hope by Promising New Drug Combination
Prof. Zhang and his colleagues from Northwestern’s Feinberg School of Medicine combined experiments in mouse models, human immune cells, and human tumor samples with analysis of large patient cancer datasets.
The mouse studies included models with triple-negative breast cancer, melanoma, ovarian cancer, colon cancer. and prostate cancer. The researchers either genetically removed CysLTR1 or blocked it using drugs such as montelukast.
In several mouse models, blocking the pathway slowed tumor growth, improved survival, and restored response to cancer-killing immunotherapy.
That worked even in tumors that had already stopped responding to treatment.
Zhang’s team also analyzed human immune cells. The findings, published in the journal Nature Cancer, again showed that blocking CysLTR1 prevented the formation of immune-suppressing neutrophils.
“Importantly, instead of simply removing these harmful white blood cells, we were able to reprogram them into cells that support immune attack.
GREAT TIP: 10 Minutes of Intensive Workout Can Trigger Powerful Anti-Cancer Effects: New Study
“That means we’re not just targeting the cancer, we’re re-training one type of abundant immune cells in the body to fight the tumor again.”
In analyses of human tumor samples and public cancer datasets, the scientists found more evidence that CysLTR1 plays a crucial role in promoting cancer growth.
They discovered that patients with higher CysLTR1 activity tended to have worse survival and poorer response to immunotherapy across multiple cancer types.
Prof. Zhang says because drugs that block CysLTR1, such as montelukast, are already FDA-approved, the findings could quickly move into patient trials.
“We may be able to quickly and safely test it in cancer patients to improve immunotherapy, especially in aggressive cancers, like triple-negative breast cancer, where new options are urgently needed.
CHECK OUT: ‘Incredibly Encouraging’ Drug Trial Shrinks Tumors in Head and Neck Cancer Patients Within Six Weeks
“The next steps are to confirm this mechanism in patients, identify who will benefit most, optimize how we use these drugs especially in combination with immunotherapy, and begin carefully designed clinical trials.”
SPREAD SOME HOPE On Social Media…