University of North Carolina scientists have engineered immune cells that can destroy acute myeloid leukemia while sparing healthy blood tissue, overcoming a limitation that has plagued standard treatments, which have struggled to separate cancerous cells from normal cells. Immunologist Gianpietro Dotti and hematologist Paul Armistead directed research teams whose work appears in the journal Blood, offering an approach that may expand options for patients battling this deadly disease.
Acute myeloid leukemia afflicts adults and children alike, with diagnoses rising steadily, particularly across America and countries experiencing population aging. The malignancy typically advances rapidly through the bone marrow and bloodstream once it develops.
Unfortunately, existing therapies damage normal blood-forming cells alongside malignant ones, creating severe treatment complications that have constrained therapeutic approaches to cancer for decades.
Research teams discovered a protein fragment named CG1 that coats leukemia cell exteriors abundantly, displayed on cellular surfaces by another molecule called HLA-A*02:01. Healthy blood cells completely lack this marker. Dotti, who directs UNC Lineberger’s Clinical Immunotherapy Program while teaching microbiology and immunology, explains that his group pursued cross-disciplinary strategies to locate safe molecular targets.
The researchers then modified human immune cells to detect minute target quantities while preventing malignant cells from evading recognition. Teams constructed chimeric antigen receptor T-cells that can spot and eliminate cells bearing the CG1/HLA-A*02:01 pairing, building on similar engineered immune cells that already demonstrate strong results against B-cell lymphoma and multiple myeloma in clinical settings.
The treatment removes patient T-cells for laboratory processing, where genetic alterations equip them to identify particular cancer markers, then reinfusion returns the modified cells so they can expand rapidly and pursue malignant targets throughout the body.
Testing in laboratory dishes and mouse experiments confirmed the altered T-cells killed leukemia samples effectively while healthy blood cells survived intact. This marks substantial progress over previous chimeric antigen receptor attempts that caused excessive harm by attacking healthy and diseased cells equally.
That toxicity prevented clinical use despite cancer-fighting capability, as the inability to distinguish friend from foe doomed earlier efforts.
Focusing on the CG1/HLA-A*02:01 pairing could enable leukemia elimination without damaging healthy surrounding cells since CG1 is completely absent on normal cells. This distinction lets engineered immune cells differentiate targets from bystanders accurately, with study results indicating CG1.CAR-T cells might benefit acute myeloid leukemia patients who currently lack targeted immunotherapy that preserves healthy tissue function.
Further research could open the door to more advanced and even side-effect-free cancer therapies, and many companies like Calidi Biotherapeutics Inc. (NYSE American: CLDI) are focused on doing just that.
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