This article has been reviewed according to Science X's editorial process and policies. Editors have highlighted the following attributes while ensuring the content's credibility: Many liver and lung cancers arise in tissue that's already been scarred by chronic disease, such as hepatitis, cirrhosis or long-term lung damage. That scarring creates an environment that suppresses nearby immune cells, so by the time a tumor takes hold, it's often already shielded from the immune system and immunotherapy.
Now, scientists at Memorial Sloan Kettering Cancer Center (MSK) have developed a new approach to breaking down this barrier. They engineered nanoparticles—tiny particles about 1,000 times smaller than the width of a human hair—that can be loaded with drugs and directed at specific cells in the body. By selectively eliminating a small population of immune cells found to drive fibrosis, the approach could make immunotherapy work for more patients with minimal toxicity to healthy cells.
The laboratory findings, published in Science, could pave the way for new approaches against immunotherapy-resistant tumors, as well as other fibrotic and inflammatory diseases. "Immunotherapy can elicit amazing therapy responses—but right now it doesn't work for the vast majority of patients," says Scott Lowe, Ph.D., a co-corresponding author of the study. "So anything we can do to make it work better and for more people is worth pursuing." The study was led by co-first authors Clemens Hinterleitner, M.D., and Valentin Barthet, Ph.D., both postdoctoral researchers in the Lowe Lab, and doctoral student Hailey Goldberg, M.S., also of the Lowe Lab.
It was additionally overseen by co-corresponding authors Aveline Filliol, Ph.D., and Daniel Heller, Ph.D. For years, Lowe's lab has been interested in a biological process called cellular senescence—a response to stress that causes cells to permanently stop dividing. "Senescence is a double-edged sword," says Lowe, who chairs the Cancer Biology and Genetics Program at MSK's Sloan Kettering Institute.
On one hand, senescence is beneficial: When cells are damaged, it can shut them down before they turn cancerous. It also plays an important role in wound healing, where senescent cells help coordinate the repair process by sending out signals that recruit other cells to the injury. But those same signals can present a problem when senescent cells stick around too long.
Rather than disappearing after doing their job, lingering cells continue broadcasting signals that drive chronic inflammation and fibrosis. This makes them an attractive therapeutic target, says Lowe, who is also a Howard Hughes Medical Institute investigator and holds the Geoffrey Beene Chair at MSK. "If we could find a way to clear out the harmful cells while leaving the helpful ones intact, we might be able to treat a wide range of conditions driven by chronic inflammation and fibrosis—including cancer," he says.
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