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The term „hematopoietic cancer” refers to several, in most cases quite severe health conditions in which the process of blood cell production is altered. Cancers of white blood cells are characterized by enhanced proliferation and reduced differentiation and cell death in one myeloid lineage, which can promote the outgrowth of a dominant myeloid cell type. The transformation to AML is the most devastating complication experienced by patients. This type of cancer usually progresses quickly and despite considerable advances in therapeutic approaches and allogeneic hematopoietic stem cell transplantation, only 26% of patients survive longer than 5 years. These conditions are frequently caused by mutations that over-activate intracellular signalling or gene transcription. Activating mutations in the receptor FLT3 represent 30% of driver mutations in AML, which in turn activates STAT5, an important transcription factor for blood cell transformation. Targeting the mutated proteins with small molecular weight drugs is currently the leading strategy for combating cancer. However, while FLT3 inhibitors induce responses in AML-patients with FLT3 mutations initially, responses are not durable, and AML progresses in virtually all patients. New treatment strategies are therefore urgently needed to improve patient survival of this aggressive disease.

Transcription factors like STAT5 are similar to genetic

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