A New Weapon Against Solid Tumors:
CAR T-cell therapy has been a genuine revolution in treating blood cancers like leukemia and lymphoma… but for solid tumors, it has largely hit a wall. Two stubborn obstacles have stood in the way: solid tumors often lack a single, consistent surface target for engineered T cells to lock onto, and they’re frequently surrounded by dense scar tissue and immune-suppressive cells that block treatment from getting through.
A new study from researchers at Memorial Sloan Kettering Cancer Center, published in Cell on March 30, 2026, takes a fresh approach to both problems at once, and the results are striking.
The key is a protein called uPAR (urokinase plasminogen activator receptor). In healthy tissue, uPAR is largely quiet, appearing mainly on a small subset of immune cells involved in wound healing. But in cancer, both tumor cells and their surrounding supportive cells ramp up uPAR production significantly. The MSK team engineered CAR T cells to target this protein, and in doing so, they attacked not just the tumor itself, but the protective “ecosystem” the tumor relies on to survive.
In laboratory models, the approach shrank lung, pancreatic, and ovarian cancers, and even cleared metastases in some experiments. In a mouse model of ovarian cancer, the uPAR-targeting CAR T cells produced durable remissions and mice that had cleared their tumors resisted developing new ones when cancer was reintroduced later, suggesting the engineered cells remained active long-term. Importantly, a single post-surgical dose of the cells also eliminated residual disease that surgery alone couldn’t fully address.
What makes this particularly promising is the breadth of the target. The researchers found uPAR was elevated in 12 out of 14 human cancer types analyzed, with especially high levels in ovarian, pancreatic, colon, lung, and brain cancers. The protein tends to mark the most dangerous, identity-shifting cancer cells, those associated with aggressive behavior, inflammation, and resistance to standard treatments.
The therapy can also be enhanced by pairing it with conventional chemotherapy agents like cisplatin, which induces a state of cellular senescence that raises uPAR levels further, making tumor cells easier for the engineered T cells to find and destroy.
The findings are still preclinical, human safety and efficacy trials are the essential next step. But the science points toward something genuinely new: a CAR T strategy that doesn’t just hunt individual cancer cells, but dismantles the entire tumor support network around them. For cancers that have long resisted immunotherapy, that could change the equation considerably.
This topic is covered in Great News podcast episode 39.
Source:
Memorial Sloan Kettering Cancer Center / Zhang et al., Cell, 2026
