Researchers examine new therapy to boost chemoimmunotherapy response for bladder cancer


If anti-inflammatory drugs are added to immunotherapy and standard chemotherapy medication, it may provide long-term termination of aggressive growth of bladder tumor, according to a proof-of-concept undertaken by cancer investigators at Cedars-Sinai.

The findings of the laboratory trials are published in Nature Communications.

Meanwhile, the previous work of the researchers finds that the combined use of chemotherapy drugs cisplatin and gemcitabine is unable to activate own immune response of the patient to cancer. In addition, chemotherapy induces the overwhelming discharge of an inhibitory signal that arrests the immune response by preventing ‘go’ signals.

The addition of anti-inflammatory drug celecoxib to gemcitabine to eliminate the brake enabled to shift the balance toward the ‘go signals’, and remove the immune response in mice in laboratory trials.

Building on earlier work, the researchers found a mechanism that may drive the immune-diminishing effect of chemotherapy and demonstrated how to prevent it, and thus activating an immune response to last longer.

The findings are significant because with the new drug combination of an anti-inflammatory drugs such as celecoxib, immunotherapy and chemotherapy potentially can amplify the chemoimmunotherapy reaction in patients with risk of muscle-invasive bladder cancer.

Clinically, muscle-invasive bladder cancer is aggressive and is more likely to spread in the body, according to analysis of the Urology Care Foundation.

Meanwhile, each year in the U.S., more than 83,000 new cases of bladder cancer are detected in men and women. About one quarter of the newly diagnosed bladder cancer cases are muscle invasive type.

In fact, since the 1940s, chemotherapy drugs are used as the main treatment for destroying cancer cells, which directly destroys the cells. However, many drugs currently used for cancer fail to cause the most efficient form of cell death termed immunogenic cell death.

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