Scientists at City of Hope, one of the largest cancer research and treatment organizations in the United States, have identified how low levels of the TET2 gene fuel the rapid growth of acute myeloid leukemia in animal models. Cell Stem Cell recently published the study.
The return of leukemia stem cells to the bone marrow microenvironment/niche is substantially enhanced by low levels of TET2, at right, compared to the wild-type version of the gene. Credit: Jianjun Chen Laboratory/City of Hope
Driving the movement of malignant stem cells from the bloodstream to the bone marrow region where they originated. This home microenvironment, called a niche, protects the cells' survival and ability to divide and self-replicate. Leading to the buildup of a methylated form of the RNA base cytosine that enhances TSPAN13 messenger RNA's stability, resulting in the increased expression of TSPAN13 proteincalled the TSPAN13/CXCR4 axis that increases malignant stem cells' return to the bone marrow niche and self-replication, thereby leading to the rapid development of leukemia.
A team led by Jianjun Chen, Ph.D., the Simms/Mann Family Foundation Chair in Systems Biology at Beckman Research Institute of City of Hope, found that TET2 deficiency sets off a cascade of biochemical changes that enhance the bone marrow cancer's ability to spread. Credit: City of Hope. More than half of patients relapse, and the five-year survival rate is only 30%. Figuring out how to destroy these cells is crucial to effectively treating the disease.
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