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Drug Doubles Immune Response Against Cancer in Trial: Study  

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In a new clinical trial, a drug induced an integrated immune response in the tumors of patients with cancer types that do not usually respond to immunotherapy, say researchers.

According to the study, published in the journal Proceedings of the National Academy of Sciences, the team hopes the potential treatment might make such tumors more responsive to the class of drugs known as immune checkpoint inhibitors.

“Checkpoint inhibitors release natural brakes on the immune system, freeing it to find and destroy cancer cells. But they generally have not been effective against cancer cells with low levels of genetic mutation.”
Tobias Janowitz, study author, University of Cambridge in the UK.

Cancer immunotherapies, which empower patients' immune systems to eliminate tumours, are revolutionizing cancer treatment. Many patients respond well to these treatments, sometimes experiencing long-lasting remissions.

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But some cancers remain difficult to treat with immunotherapy, and expanding the impact of the approach is a high priority.
In this clinical trial, the research team interrupted that immunosuppressive pathway with a drug called plerixafor.

The drug was administered continuously by intravenous therapy (IV) for one week to 24 patients with either pancreatic cancer or colorectal cancer with a low tumor mutational burden.

All patients had advanced disease, and biopsies were collected from metastatic tumors before and after treatment.

When the team analyzed those patient samples, they found that critical immune cells had infiltrated the tumors during the time patients received plerixafor, including a cell type known to summon and organize key players in the anti-cancer response.

The finding was encouraging because the team detected changes that have also been observed in patients whose cancers responded well to checkpoint inhibitors, the authors wrote.

(This story was published from a syndicated feed. Only the headline and picture has been edited by FIT)

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