Memorial Sloan Kettering researchers described a new CAR T strategy aimed at uPAR-positive tumor ecosystems, seeking to expand solid-tumor targeting beyond single tumor-cell antigens. In preclinical experiments reported in Cell, the approach showed elevated uPAR expression across most of 14 analyzed cancer types and linked higher uPAR levels to fibrosis- and inflammation-associated pathways. The therapy selectively eliminated solid tumor cells alongside supportive fibroblasts and immunosuppressive myeloid cells in mouse models. Investigators also reported improved outcomes when combined with senescence-inducing treatment such as cisplatin and described durable remissions in an ovarian cancer model. The findings position uPAR as a potential multiplexing target, reinforcing the broader field shift toward CAR T designs that neutralize both malignant and supporting microenvironment cell populations.
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