Bold claim first: a breakthrough approach may halt leukemia stem cell growth by tweaking cellular signals in the bone marrow. But here’s where it gets controversial: can tweaking these signals really stop cancer without unintended side effects? This rewrite preserves all key points and clarifies the ideas for beginners, while expanding slightly for context and readability.
A new study published in Nature Communications from a research team at the University of Oslo investigates how cancer cells form in the bone marrow and whether their growth can be stopped. The researchers report a method to halt malignant stem cells and suggest their findings could open up new avenues for future treatments.
According to Lorena Arranz, Associate Professor at the University of Oslo and leader of the Stem Cells, Ageing and Cancer group (also Deputy Director at the Centre for Embryology and Healthy Development, CRESCO), the team aims to improve detection and treatment of leukemia. She notes that the study provides fresh insights into acute myeloid leukemia and that the results could inform the development of new therapies.
The study demonstrates that leukemia development can be influenced in mouse models. The team focused on blood stem cells in the bone marrow, which can either stay dormant or actively divide to form new blood cells. In healthy individuals, these cells mature into red blood cells, white blood cells, and platelets. In acute blood cancer, however, stem cells may become cancerous instead of healthy blood cells. The researchers believe it may be possible to prevent this switch by understanding the signaling environment surrounding stem cells.
Arranz states that they have identified signals that influence leukemia development and could be exploited to fight the cancer. These signals help maintain a balance, directing stem cells to remain dormant or to generate new cells. The study identifies specific molecules—succinate and its receptor SUCNR1—and explains how their levels affect whether stem cells accelerate growth or slow down. Activation of SUCNR1 appears to keep stem cells healthy by regulating alarmins S100A8 and S100A9.
The researchers examined patient data from individuals with acute myeloid leukemia and conducted experiments in mouse models using advanced techniques such as stem cell analyses, RNA sequencing, and spectral flow cytometry.
In patient samples, low SUCNR1 expression correlated with poorer survival. In mouse models, the researchers observed that altering succinate, SUCNR1, and S100A9 levels could influence leukemia progression. Arranz and colleagues demonstrated that adjusting these factors could steer leukemia development in mice.
The researchers see potential for new treatments for acute myeloid leukemia. Arranz is optimistic about the path forward, noting that succinate has often been viewed as a driver of cancer progression. In this study, succinate shows a protective role via SUCNR1, offering a potential therapeutic angle to explore.
Vincent Cuminetti, the study’s first author, also highlights future possibilities for personalized treatments based on SUCNR1 levels. The team envisions leveraging these findings to design targeted therapies for patients with specific SUCNR1 expression profiles.
Source:
Cuminetti, V., et al. (2026) Succinate receptor 1 restricts hematopoiesis and prevents acute myeloid leukemia progression. Nature Communications. DOI: 10.1038/s41467-026-68906-2.
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