Two days after a University of Southern California–led team published a landmark USC GMP expansion Cell paper, the field of cancer immunotherapy is grappling with a finding that challenges one of hematopoiesis’s most durable assumptions: that long-term self-renewal belongs only to stem cells.
In a study published June 29, 2026, researchers led by Qi-Long Ying, MD, PhD, at the Keck School of Medicine of USC showed that granulocyte-monocyte progenitors — the intermediate immune cells that give rise to macrophages — can be chemically coaxed into dividing indefinitely in the laboratory while retaining their identity and full biological potential. The team then engineered those progenitors to hunt cancer, injected them into tumor-bearing mice, and showed that the cells engrafted in the bone marrow, continuously replenished an anti-tumor macrophage supply, and slowed disease progression in both blood cancers and solid tumors. A separate Stanford University laboratory independently reproduced the core findings, and the technology has already been licensed to Myelogene Inc., a spinout co-founded by members of both research teams.
Why CAR-T Has Struggled Against Solid Tumors — and Why Macrophages Are Different
Chimeric antigen receptor T-cell therapy has produced remissions that would have seemed impossible a decade ago, but almost exclusively in blood cancers. Since the first FDA-approved CAR-T therapies product (tisagenlecleucel, 2017), every approved therapy has targeted leukemia, lymphoma, or multiple myeloma.
Solid tumors — which account for approximately 90 percent of all cancer diagnoses — have proven far more resistant. The reasons are structural: T cells struggle to physically penetrate the dense extracellular matrix around solid tumors, they exhaust rapidly inside the immunosuppressive tumor microenvironment, and they lack the surface-antigen targets that blood cancer cells display so cleanly. CAR-T barriers in solid tumors are well documented in the recent literature…