A new study published this week in Immunity could change the way oncologists tailor treatments to a patient's specific type of tumor.
A team of scientists at Penn Medicine's Abramson Cancer Center looked at why tumors with more T cells, or cells that play a vital role in the immune response, are more sensitive to immunotherapy than those with fewer T cells. Those with more of these cells are known as "hot" tumors and those with less are known as "cold."
The researchers looked at the role of "tumor heterogeneity," a cancer cell's ability to move, replicate, metastasize and respond to treatment. They found that whether a tumor is hot or cold is determined by information embedded in the cancer cells themselves.
Recent findings from Penn Medicine and other institutions have suggested that whether T cells are attracted to a tumor is regulated by genes specific to that tumor. In simpler terms, they found that the tumor's immunity is controlled by factors that are specific to the individual cancer cells.
"There is no disputing that targeting immune cells has led to promising outcomes for many cancer patients, but not every person responds to these types of treartments," lead author Ben Stanger, a professor of Gastroenterology and Cell and Developmental Biology in the Perelman School of Medicine at the University of Pennsylvania, said in a press release. "Every tumor is different, so we're investigating how to use the underlying biology of tumor cells to successfully treat more cancer patients."
The findings would mean tailoring a patient's treatment to best kill off cancer cells. To grow, tumors need to avoid the immune system, which happens in two ways: by developing as a cold tumor with a limited number of T cells, or as a hot tumor by exhausting the T cells, effectively protecting tumor cells from destruction by a patient's immune system.
For the study, scientists implanted cancer cells into mice. The cells grew into hot or cold tumors, with cold tumors being the dominant type. They found that whether a tumor was hot or cold determined whether it would respond to immunotherapy.
Hot tumors shrunk in half of the mice when a checkpoint blockade drug was used. The effect was enhanced with either an anti-CD40 agonist, combined chemotherapy or both. Of the 26 mice on which these methods were used, 20 survived more than six months. This suggests a durable response to the therapy.
None of the mice with the cold tumors cleared their cancer following this therapy.
The findings gave the scientists a clearer profile of the features of pancreatic tumors, including the types of immune cells they contain. In the future, these cell lines could help to identify and optimize therapies for specific patients.
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