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Please use this identifier to cite or link to this item: http://hdl.handle.net/1807/17699

Title: Hyper-methylation of the SOCS2 Promoter in AML: An Unexpected Association with the FLT3-ITD Mutation
Authors: McIntosh, Courtney
Advisor: Minden, Mark
Department: Medical Biophysics
Keywords: Leukemia
Methylation
Issue Date: 22-Sep-2009
Abstract: Haematopoiesis requires strict regulation in order to maintain a balanced production of the various blood cell components. Escape from this regulation contributes to the development of cancers such as leukemia. SOCS2 is a member of the Suppressor of cytokine signalling (SOCS) family, and normally functions as a negative regulator of the JAK/STAT pathway. I examined gene expression and promoter methylation in acute myeloid leukemia (AML) cell lines and patient samples. SOCS2 expression was quite variable in AML patients, and very low in acute promyelocytic leukemia (APL) patients. Promoter hyper-methylation was found in these patients, particularly those with high white blood cell count and a FLT3-ITD. I speculate that SOCS2 interacts with an aspect of the signalling complex to inhibit cell growth in these patients, and silencing SOCS2 is necessary for leukemia progression. Treating these patients with a de-methylating agent, such as decitabine, may show promise in the clinic.
URI: http://hdl.handle.net/1807/17699
Appears in Collections:Master
Department of Medical Biophysics - Master theses

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