Rethinking the Biology of Chronic Myeloid Leukemia
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By
February 11, 2026
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2 min
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1
CML historically viewed as driven by oncogene translocation.
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2
Van Etten's findings highlight necessity of malignant stem cell accumulation.
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3
Preclinical mouse model utilized for research validation.
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4
New model reshapes understanding of leukemogenesis.
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5
Insights provoke reassessment of risk stratification and interventions.
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6
Systems biology at UCI revolutionizes traditional cancer models.
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7
Study supports threshold-based understanding across cancer types.
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At ASH 2025, Richard Van Etten, MD, PhD, presented transformative insights from the UCI Center for Cancer Systems Biology regarding the development of chronic myeloid leukemia (CML). Historically seen as driven by a specific chromosomal translocation creating an oncogene, Van Etten's research reveals that this mutation is necessary but not sufficient for disease progression. The studies utilize a preclinical mouse model, discovering that accumulation of malignant stem cells is critical for CML development, reshaping our understanding of leukemogenesis and its implications for early intervention and risk assessment.
-
1
CML historically viewed as driven by oncogene translocation.
-
2
Van Etten's findings highlight necessity of malignant stem cell accumulation.
-
3
Preclinical mouse model utilized for research validation.
-
4
New model reshapes understanding of leukemogenesis.
-
5
Insights provoke reassessment of risk stratification and interventions.
-
6
Systems biology at UCI revolutionizes traditional cancer models.
-
7
Study supports threshold-based understanding across cancer types.
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