SALL4, a novel oncogene, is constitutively expressed in human acute myeloid leukemia (AML) and induces AML in transgenic mice
作者： Y. Ma , W. Cui , J. Yang , J. Qu , C. Di
DOI: 10.1182/BLOOD-2006-02-001594
关键词:
摘要: SALL4, a human homolog to Drosophila spalt, is novel zinc finger transcriptional factor essential for development. We cloned SALL4 and its isoforms (SALL4A SALL4B). Through immunohistochemistry real-time reverse-transcription-polymerase chain reaction (RT-PCR), we demonstrated that was constitutively expressed in primary acute myeloid leukemia (AML, n = 81), directly tested the leukemogenic potential of constitutive expression murine model. SALL4B transgenic mice developed myelodysplastic syndrome (MDS)-like features subsequently AML transplantable. Increased apoptosis associated with dysmyelopoiesis evident mouse marrow colony-formation (CFU) assays. Both could bind β-catenin synergistically enhanced Wnt/β-catenin signaling pathway. Our data suggest causes MDS/AML, most likely through model provides useful platform study MDS/AML transformation, as well pathway's role pathogenesis stem cells.
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