, and a HER2 receptor. The absence of any of these receptors—receptors that when present in other forms of breast cancer, can be effectively targeted during treatment—makes treating TNBC quite difficult, and patients with TNBC have limited treatment options.
But Schug and co-authors have demonstrated the efficacy of a double-acting concept: Silencing the gene ACSS2 impairs TNBC metabolism while simultaneously boosting the immune system's ability to fight it. ACSS2 regulates acetate, a nutrient that cancer cells—and TNBC cells in particular—take advantage of to grow and spread.
This process of guiding the immune system to the cancer—called"immunosensitization"—has confounded other TNBC researchers. But Schug's approach showed that ACSS2 inhibition immunosensitized against TNBC so well that tumor growth was drastically reduced, even to the point of wiping out the cancer completely in some experiments.
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