This subproject is one of many research subprojects utilizing theresources provided by a Center grant funded by NIH/NCRR. The subproject andinvestigator (PI) may have received primary funding from another NIH source,and thus could be represented in other CRISP entries. The institution listed isfor the Center, which is not necessarily the institution for the investigator.The pathogenesis of acute myeloid leukemia (AML) involves a progressive set of genetic alterations via activation of proto-oncogenes or inactivation of tumor suppressors. Dr. Ma has discovered a new oncogene, SALL4, which is constitutively expressed in human leukemia cell lines and almost 100% of primary acute myeloid leukemia cells. Transgenic mice overexpressing SALL4B exhibited myelodysplastic (MDS)-like feactures and subsequently, acute myeloid leukemia (AML) transformation. In addition, PI has shown that SALL4A and SALL4B are able to bind to -catenin, an essential component for Wnt signal pathway. The hypothesis underlying this project is that aberrant constitutive expression of SALL4 is oncogenic in AML. To test this hypothesis, the specific aims of this project are as follows:
Specific Aim I : Determine molecular mechanism(s) of SALL4 isoforms in the initiation and/or the progression of AML.
Specific Aim II : Determine how SALL4 isoforms affect signaling pathways, which initiate or cause progression of AML. These studies will provide detailed information on the role played by SALL4 isoforms in AML. The knowledge obtained will provide a better understanding of hematopoietic cell differentiation and leukemogenesis, and may lead to the identification of novel therapeutic targets for AML.
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