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Augmenting the Immune System to Achieve Great Outcomes in Cancer Care

Laura Joszt
During the session "Principles of Immunotherapy" at the National Comprehensive Cancer Network 20th Annual Conference in Hollywood, Florida, Anthony J. Olszanski, RPh, MD, from the Fox Chase Cancer Center, described the complex interplay between the immune system and cancer.
During the session “Principles of Immunotherapy” at the National Comprehensive Cancer Network 20th Annual Conference in Hollywood, Florida, March 12-14, 2015, Anthony J. Olszanski, RPh, MD, from the Fox Chase Cancer Center, described the complex interplay between the immune system and cancer.

He began with a basic explanation of the history of immunotherapy, noting how because cancer commonly grows from our cells, the immune system often considers them as “self” and does not reject the cancer. Because all cancers inevitably result in a genetic defect at some point, the immune system is then able to differentiate and recognize the antigens being produced by the cancer cells. “So even though tumors are ‘self,’ they have mutations,” Olszanski said. “Those mutations are producing mutated proteins or over-expressing them, which might result in an antigen presenting itself as a non-self antigen.” He went on to highlight a recent article in the New England Journal of Medicine by Snyder et al1 reporting on a study which found that melanoma patients with more than 100 mutations had a better survival rate compared with patients with fewer mutations.

Olszanski also described the immunoediting hypothesis, which explains why cancer progression can vary in patients. There is the illumination phase, in which active immune surveillance recognizes the tumor and eradicates it; the equilibrium phase, during which the cancer is not growing as quickly because there is a balance between tumor progression and the immune system trying to suppress that progression; and finally, the escape mechanism, where either reduced immunogenicity prevents the immune system from finding the cancer effectively or the cancer grows faster than the immune system can suppress it.

“So the immunoediting hypothesis really helps explain how some of our patients seem to do exceedingly well, might get complete remissions, and never come back; other patients seems to have stable disease; and some other patients seem to escape it completely,” he explained. He went on to describe some of the immunotherapies currently available that are expanding knowledge of both the immune system and diseases. For instance, he said, PD-1 inhibitors have captured a great deal of attention because they have been widely useful in a variety of cancers (eg, the use of nivolumab in non-Hodgkin lymphoma), bringing about some reduction in the tumor burden of every patient. In addition, the PD-L1 antibody, MEDI4736, has shown activity in a wide variety of cancers, including pancreatic cancer.

“Can we imagine another therapeutic option for our pancreatic cancer patients who have to go through the chemotherapy that we currently give them today?” he asked. “If immunotherapy works in that patient population, I can say that we’ve really made some headway against one of the most devastating diseases that we currently have out there.”

Reference

1. Snyder A, Makarov V, Merghoub T, et al. Genetic basis for clinical response to CTLA-4 blockade in melanoma. N Engl J Med. 2014; 371:2189-2199.

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