Scientists from the Institute of Wilmot Cancer figure out how EVI1 gene is responsible for the development of acute myeloid leukemia (AML), a deadly type of cancer. This gives hope that treatment aimed at genes that can improve survival rates in AML.
Due immunotherapy approaches, and other targeted treatment of many types of blood cancer has improved, but patients with AML are all also have lower survival rates. Only 25% of patients with acute myeloid leukemia survive for three years. While some patients may achieve long-term remission due to a bone marrow transplant and blood, the disease almost always recurs.
Scientists around the world are exploring EVI1 gene, considering its relationship with leukemia "from all sides", to improve the treatment of these patients. This gene is characterized by overexpression in AML. EVI1 alters the metabolism of blood immature cells when they become cancerous.
Gene EVI1 «twist around" the totality of hematopoietic cells and tissues by binding to specific DNA molecules and "causing" chaos. Knowing where in the genome is fixed EVI1, it helps scientists to better understand the mechanisms that lead to the development of the disease.
Scientists note that a new study:
- It shows in detail how the disturbance in the circulatory system leads to increased concentrations of myeloid cells, displacing healthy red blood cells, which transport oxygen and fight infection. Myeloid cells eventually support the development of leukemia in the bone marrow.
- Uses the model mice with a disease closely mimics AML in humans;
- It demonstrates how and where EVI1 binds to specific DNA molecules and begins to cause problems.
Now scientists can start working on a new approach in the treatment of AML based on blocking ability EVI1 communicate with other genes.