Scientists have identified a molecule that can be targeted to reprogram immune cells, transforming them into agents that promote cancer.
Cancer has been metaphorically referred to as “a wound that does not heal,” suggesting that the immune system struggles to eliminate invasive tumor cells. Recent findings reveal that a crucial molecule can alter immune cells, typically responsible for defending against infections and cancer, into their harmful equivalents that facilitate cancer progression.
Researching the behavior of these “pro-tumor” immune cells is vital since they may serve as potential targets for therapies designed to inhibit their adverse actions, according to Minsoo Kim, PhD, the study’s lead author and a research leader at the Wilmot Cancer Institute.
The discovery was published in the Proceedings of the National Academy of Sciences (PNAS).
Kim spearheaded a group of researchers examining the intricate interactions between cells in the tumor environment and the factors that trigger the detrimental shift of immune cells from protective to harmful roles.
They identified PAF (platelet-activating factor) as the critical molecule that determines the fate of immune cells.
PAF not only attracts cells that promote cancer but also inhibits the immune system’s ability to counteract the cancer. Furthermore, the researchers discovered that various cancers depend on these PAF signals.
“This could be particularly important,” noted Kim, a Dean’s Professor of Microbiology and Immunology at the University of Rochester Medical Center. “If we can develop a treatment that disrupts PAF, it may have implications across multiple cancer types.”
A significant portion of the research concentrated on pancreatic cancer, which is among the deadliest cancers, with a five-year survival rate of around 12 percent. This type of cancer is particularly challenging to treat because pancreatic tumors are shielded by a toxic mix of proteins and tissues, allowing the cancer to evade the immune system’s natural attack mechanisms. The team also investigated breast, ovarian, colorectal, and lung cancer cells, utilizing advanced 3D imaging technology to observe how immune cells react and move toward cancerous areas.
Ankit Dahal, PhD, a member of Kim’s lab and a student in the UR Medical Scientist Training Program, developed the research project and collaborated with Kim on the journal article.
The study received funding from the National Institutes of Health.
As the director of tumor immunotherapy research at Wilmot, Kim explores various facets of the immune system and its relationship with cancer. He works alongside other Wilmot researchers and leaders, including Darren Carpizo, MD, PhD; Scott Gerber, PhD; and David Linehan, MD, the CEO of URMC, all of whom are involved in pancreatic cancer research. Additionally, Kim is collaborating with clinician-scientist Patrick Reagan, MD, as part of a grant aimed at enhancing CAR T-cell immunotherapy, an effective treatment for blood cancers.
