Some tumors do more than hide from the immune system. They can actually manipulate immune cells into helping cancer survive and spread. Now, researchers say an asthma drug may be able to interrupt that process.
In a new study published in Nature Cancer, researchers at Northwestern Medicine found that many tumors appear to use a molecule called CysLTR1 to suppress immune attacks. When researchers blocked that pathway using montelukast in preclinical models, the generic version of the asthma drug Singulair®, tumor growth slowed across several cancer types, and some tumors began responding to immunotherapy again.
This could be especially important for aggressive cancers like triple-negative breast cancer, where immunotherapy often does not work as well as doctors hope.
“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 Bin Zhang in a press release.
How an Asthma Drug Helped Tumors Respond to Immunotherapy Again
At the center of the discovery are neutrophils, white blood cells that the body quickly produces during infections and injuries. Tumors appear able to redirect that emergency response to generate large numbers of immune-suppressing cells.
When researchers blocked CysLTR1 in mice, the immune system seemed better able to recognize and attack tumors.
Explore All OptionsThe effect showed up across multiple cancers, including triple-negative breast cancer, melanoma, ovarian cancer, colon cancer, and prostate cancer.
In several cases, tumors that had stopped responding to anti-PD1 immunotherapy began responding once more. Anti-PD1 drugs work by removing some of the biological “brakes” cancers use to keep immune cells from attacking tumors, though many cancers eventually adapt and become resistant.
CysLTR1 may help drive part of that resistance, potentially giving researchers a new target to make immunotherapy effective for longer periods.
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The Asthma Drug Did More Than Slow Tumor Growth
The treatment did not just destroy the problematic immune cells. Instead, it appeared to push them out of their tumor-protecting role.
“Instead of simply removing these harmful white blood cells, we were able to reprogram them into cells that support immune attack,” Zhang explained. “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.”
Because neutrophils help fight infections, preserving them may help avoid weakening normal immune defenses.
The team combined mouse experiments with studies of human immune cells, tumor samples, and large cancer patient datasets.
The researchers also found that patients with higher CysLTR1 activity tended to have poorer responses to immunotherapy and worse survival rates across multiple cancer types.
Why the Findings Could Move Quickly Into Human Trials
Because doctors have prescribed montelukast for asthma and allergies for years, the drug could move into cancer trials much faster than an entirely new treatment, since we already understand much of the drug’s safety profile and side effects.
The next step is figuring out which patients are most likely to benefit and how drugs like montelukast might work alongside existing immunotherapy treatments before moving into clinical 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,” Zhang said.
This article is not offering medical advice and should be used for informational purposes only.
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Article Sources
Our writers at Discovermagazine.com use peer-reviewed studies and high-quality sources for our articles, and our editors review for scientific accuracy and editorial standards. Review the sources used below for this article:
- This article references information from a study published in Nature Cancer: Targeting cysteinyl leukotriene receptor 1 reprograms tumor-promoting myelopoiesis and overcomes immune checkpoint therapy resistance
