Cancer

Chemotherapy Treatment May Be Transformed Into Drug That Kills Cancer Cells, Study Says

The combination of two drugs delivered a "one-two punch" of killing tumor cells and activating immune cells, said Keith Syson Chan, a Cedars-Sinai translational scientist and the study's corresponding author.

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A study released Monday by investigators from Cedars-Sinai Medical Center shows the potential of transforming a commonly used chemotherapy drug into one that kills cancer cells by activating immune cells when it is paired with anti-inflammatory medication.

Researchers said they discovered that the chemotherapy drug gemcitabine converted from a non-immunogenic drug -- which is not able to activate a patient's own immune response -- to an immunogenic drug that triggered the immune response in mice when the anti-inflammatory medicine celecoxib (Celebrex) was added.

The combination of the two drugs delivered a "one-two punch" of killing tumor cells and activating immune cells, said Keith Syson Chan, a Cedars-Sinai translational scientist and the study's corresponding author.

"I believe that our study has significant clinical potential, as cancer immunotherapy continues to emerge as an important pillar for treating cancer patients," Chan said. "This discovery, if confirmed in clinical trials, may potentially increase the percentage of patients who respond to cancer immunotherapy."

About 70% to 85% of patients currently taking immunotherapy drugs fail to respond to them, according to Chan.

Chan and the study's first author, Kazukuni Hayashi, said they believe the immune response will perform even better if an immunotherapy drug is added to a gemcitabine and celecoxib treatment regimen, with a study underway in Chan's laboratory to test that hypothesis.

"Harnessing the patients' immune system to attack patients' tumor cells has become an important tool for physicians treating cancer," said Dr. Dan Theodorescu, director of the Cedars-Sinai Cancer enterprise. "Unfortunately, our current efforts fail in a significant number of patients. This study unveils at least one potential mechanism explaining these failures, and more importantly, provides a potential solution."

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The findings, made in human and mouse cancer cells and laboratory mice, were published in the peer-reviewed journal Nature Communications.

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