Leukemia Cells are Addicted to a Healthy Gene
Pre-leukemic stem cells (top) with both mutated and healthy copies of the RUNX1 gene already display some of the characteristics of acute myeloid leukemia (AML). When the non-mutated copy of the gene is inactivated, disruptions in the spindle-assembly-checkpoint phase of cell division trigger cell death
The present study was mainly conducted by postdoctoral fellow Dr. Oren Ben-Ami in Groner’s lab, together with the group of Dr. Amos Tanay of the Computer Science and Applied Mathematics Department and Dena Leshkowitz of the Israel National Center for Personalized Medicine. In preparation for their research, the scientists were searching in various bimolecular databases for information. That is when they noticed something unusual: The clinical data suggested that the second copy of the RUNX1 gene – the healthy, non-mutated gene – in the leukemic cells was always preserved and even highly functional. Of course, almost all the genes in our cells are doubles – one copy from each parent – and the mutations that lead to cancer are likely to occur in only one of those genes. But somewhere along the path leading to full blown cancer, the healthy genes commonly tend to get silenced or overruled and the mutated ones end up prevailing.
Dr. Amos Tanay’s research is supported by Pascal and Ilana Mantoux, Israel/France; the Wolfson Family Charitable Trust; the Rachel and Shaul Peles Fund for Hormone Research; and the estate of Evelyn Wellner. Dr. Tanay is the incumbent of the Robert Edward and Roselyn Rich Manson Career Development Chair in Perpetuity.
Weizmann Institute of Science