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$2.3 million in NIH funding for promising cancer research at Cincinnati Children's
Date:4/15/2010

studying molecular mechanics of how Fanconi anemia (FA) proteins regulate cell response to oxidative stress during hematopoiesis, the process of blood cell formation in bone marrow. This is important to understanding the progression Fanconi anemia, bone marrow failure, myelodisplastic syndrome (once called pre-leukemia), AML and the underlying genomic instability in people with Fanconi anemia.

The researchers have already shown that bone marrow cells from patients with Fanconi anemia accumulate high levels of molecules called reactive oxygen species (ROS). ROS molecules are the source of oxidative stress and bone marrow cells in people with Fanconi anemia are sensitive to ROS suppressing the formation of blood stem and progenitor cells. The scientists have also demonstrated that abnormal accumulation of ROS leads to formation of leukemic cells in a mouse model of Fanconi anemia. The team has reported that a specific FA protein, FANCD2, binds and works with the transcription factor FOXO3a, which helps control the transfer of genetic information in cellular stress response processes. Together hey form a complex that helps provide a cellular defense system against oxidative stress.

By using cells from children with Fanconi anemia and working with mouse models in their continued research, the scientists hope to find new therapeutic targets to treat or prevent bone marrow failure and related cancer progression.


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Contact: Nick Miller
nicholas.miller@cchmc.org
513-803-6035
Cincinnati Children's Hospital Medical Center
Source:Eurekalert

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