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"Gene Addiction" of Leukemia Cells If Targeted Could Prevent Disease Development
The team, led by Dr Veronika Sexl from the University of Vienna, conducted their research on acute lymphoid leukemia (ALL) and chronic myelogenous leukemia (CML), which can both be caused by fusion protein, Bcr-Abl, created through the joining of two or more genes originally coded for separate proteins.
This joining of genes results in a complex tumor supporting 'network', which supports the growth and survival of the leukemic cells.
Inhibitor drugs such as 'Imatinib' can block vital signals and lead to leukemia cell death, but there are several mutations, which can resist these inhibitors, making them ineffective.
As an alternative strategy, the team investigated transcription factors Stat3 and Stat5, which are linked to bcr/abl-induced transformation.
The team tested whether Stat3 and Stat5, acting downstream of Bcr-Abl are critical for leukemia maintenance and if they could be a alternative target for treatment.
"We developed a tumors-specific gene-deletion approach to analyze the roles of Stat5 and Stat3 in Bcr/Abl-induced leukemia growth. We discovered that both factors are required for the development of Bcr-Abl, but once established only Stat5 is crucial for the survival and growth of leukemic Cells," said Sexl.
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More News on: Leukemia, Parkinsons Disease Surgical Treatment, Chronic Myeloid Leukemia, Acute Myeloid Leukemia, Acute Lymphoblastic Leukemia, Multiple Myeloma, Bone Marrow Transplantation
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