Interferon-alpha pushes blood stem cells down two opposing paths in myeloproliferative neoplasms
Lama C and colleagues tracked how interferon-alpha treatment reshaped blood cell development in patients with myeloproliferative neoplasms in 2026. The therapy pushed blood stem cells into two opposing states at once: one that expanded anti-inflammatory lymphoid progenitors, and one that produced inflammatory myeloid progenitors. The lymphoid expansion offset the myeloid bias typical of the disease, and blood counts normalized. Single-cell multiomics revealed that stem cells carrying CALR or JAK2 mutations resisted turning into inflammatory myeloid progenitors, which let the mutated clones hold onto their fitness advantage.
Interferon-alpha is the only therapy known to deplete mutated stem cells in myeloproliferative neoplasms. Knowing that CALR- and JAK2-mutated cells survive treatment by dodging the inflammatory myeloid path gives clinicians a mechanism to explain, and potentially target, why some patients' mutated clones persist.
Written by the Genomes desk from the primary source cited and linked above and checked against it. Research use only; not medical advice. Corrections: [email protected].