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We have discovered that transcription factor SALL4, an embryonic stem (ES) cell gene and leukemic stem cell factor, belongs to a new class of oncofetal gene. It is a unique link between normal stem cells and cancer cells including leukemic initiating cells (LICs).

SALL4 is essential for ES cell and development and is aberrantly expressed in many human cancers. Gain-of-function SALL4 transgenic mice develop myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML), as well as liver tumors.  Loss-of-function studies demonstrated that SALL4 is essential for the survival of cancer cells by regulating multiple survival pathways. 

The lab currently focuses on two main projects related to SALL4’s roles in stem cells and cancer:

SALL4 in normal development and stem cell

Tatetsu et al. “SALL4, the missing link between stem cells, development and cancer”, Gene, 2016.

SALL4 in normal development

Differential functions of SALL4 in normal and leukemic hematopoiesis. While the main functional role of SALL4 in normal hematopoiesis is to maintain hematopoietic stem/progenitor cell (HSPC) proliferation and to block myeloid differentiation, the major function of SALL4 in leukemic cells is to promote cell survival. Downregulation of SALL4 expression in normal HSPCs induces differentiation; however, downregulation of SALL4 in leukemic cells triggers  apoptosis and cell death.

Wang et al. “The next new target in leukemia: The embryonic stem cell gene SALL4” Molecular & Cellular Oncology, 2014. 

SALL4 in cancer dysregulation

Yong et al. “Oncofetal gene SALL4 in aggressive hepatocellular carcinoma”, N Engl J Med, 2013.

SALL4 in cancer dysregulation
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