(Photo by Tima Miroshnichenko via Pexels)
By Stephen Beech
A drug often used to treat asthma and allergies may also help fight aggressive cancers, according to new research.
The American 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 — such as triple-negative breast cancer — where immunotherapy often fails.
And the breakthrough could quickly move into clinical testing because the drug, montelukast — commonly known by the brand name Singulair, is already approved by the U.S. Food and Drug Administration (FDA).
The research team from Northwestern University, 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.
Dr. Bin Zhang Medicine/Hematology-Oncology. (Michael Parra via SWNS)
The Northwestern team found that many cancers exploit CysLTR1 to resist treatment.
Specifically, the scientists found that tumors trick the immune system into helping them grow by increasing a group of white blood cells called neutrophils.
They discovered the protest is controlled by the CysLTR1 molecule, which acts as an on/off switch.
Study senior author Bin Zhang said: "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."
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.
(Photo by Nikolett Emmert via Pexels)
In several mouse models, blocking the pathway slowed tumor growth, improved survival and restored response to 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.
Zhang said: "Importantly, instead of simply removing these harmful white blood cells, we were able to reprogram them into cells that support immune attack.
"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.
Zhang says because drugs that block CysLTR1, such as montelukast, are already FDA-approved, the findings could quickly move into patient trials.
He added: "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.
"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."




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