SALL4, a novel oncogene, is constitutively expressed in human acute myeloid leukemia (AML) and induces AML in transgenic mice

Ma, Yupo; Cui, Wei; Yang, Jianchang; Qu, Jun; Di, Chunhui; Amin, Hesham M.; Lai, Raymond; Ritz, Jérôme; Krause, Diane S.; Chai, Li

doi:10.1182/blood-2006-02-001594

Cited by 201 publications

(323 citation statements)

References 47 publications

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“…Therefore, constitutive expression of SALL4 causes MDS, respectively, AML most probably through the Wnt/b-catenin pathway. 125 In CML SALL4 expression was absent in the chronic phase, became detectable in the accelerated phase only in immature blasts, and was strongly positive in the blast phase, 125 a situation strongly resembling AML.…”

Section: Other Mechanisms Of Aberrant Wnt Signaling In Amlmentioning

confidence: 99%

“…Recently, Ma et al 125 detected that SALL4 is an oncogene that is constitutively expressed in AML. In humans, the SALL gene family is involved in normal development, as well as in tumorigenesis.…”

Section: Other Mechanisms Of Aberrant Wnt Signaling In Amlmentioning

confidence: 99%

“…SALL4B transgenic mice developed myelodysplastic syndrome (MDS)-like features and subsequently AML. 125 Two isoforms of SALL4, SALL4A and SALL4B could bind to bcatenin and synergistically enhanced the Wnt/b-catenin signaling pathway. In addition, SALL4 is directly activated by TCF/LEF within the canonical Wnt signaling pathway.…”

Section: Other Mechanisms Of Aberrant Wnt Signaling In Amlmentioning

confidence: 99%

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The emerging role of Wnt signaling in the pathogenesis of acute myeloid leukemia

Steffen

Berdel

et al. 2007

Leukemia

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Wnt signaling plays an important role in stem cell self-renewal and proliferation. Aberrant activation of Wnt signaling and its downstream targets are intimately linked with several types of cancer with colon cancer being the best-studied example. However, recent results also suggest an important role of Wnt signaling in normal as well as leukemic hematopoietic stem cells. Aberrant activation of Wnt signaling and downstream effectors has been demonstrated in acute myeloid leukemia. Here, mutant receptor tyrosine kinases, such as Flt3 and chimeric transcription factors such as promyelocytic leukemia-retinoic acid receptor-a and acute myeloid leukemia1-ETO, induce downstream Wnt signaling events. These findings suggest that the Wnt signaling pathway is an important target in several leukemogenic pathways and may provide a novel opportunity for targeting leukemic stem cells.

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Section: Other Mechanisms Of Aberrant Wnt Signaling In Amlmentioning

confidence: 99%

Section: Other Mechanisms Of Aberrant Wnt Signaling In Amlmentioning

confidence: 99%

Section: Other Mechanisms Of Aberrant Wnt Signaling In Amlmentioning

confidence: 99%

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The emerging role of Wnt signaling in the pathogenesis of acute myeloid leukemia

Steffen

Berdel

et al. 2007

Leukemia

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“…13,16,17 For example, SALL4 expression is correlated with a poor prognosis in AML patients. 18,19 SALL4 is also found to be a biomarker for a subclass of hepatocellular carcinoma with an aggressive phenotype. 20 Through physical and/or functional interaction with OCT4, SOX2, and NANOG, SALL4 plays an essential role in maintaining pluripotency and self-renewal of embryonic stem cells and hematopoietic stem cells.…”

Section: Introducitonmentioning

confidence: 99%

Identification of the nuclear localization signal of SALL4B, a stem cell transcription factor

Yang

Ren

et al. 2014

Cell Cycle

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“…67,134,135 Interestingly, transgenic mice expressing the SALL4B isoform under the control of the CMV promoter develop MDS-like features within 6-8 months, with dysplastic neutrophils, erythrocytes and megakaryocytes, as well as increased blast counts leading to AML transformation in 50% of mice.…”

mentioning

confidence: 99%

Engineering mouse models with myelodysplastic syndrome human candidate genes; how relevant are they?

2012

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Myelodysplastic syndromes represent particularly challenging hematologic malignancies that arise from a large spectrum of genetic events resulting in a disease characterized by a range of different presentations and outcomes. Despite efforts to classify and identify the key genetic events, little improvement has been made in therapies that will increase patient survival. Animal models represent powerful tools to model and study human diseases and are useful pre-clinical platforms. In addition to enforced expression of candidate oncogenes, gene inactivation has allowed the consequences of the genetic effects of human myelodysplastic syndrome to be studied in mice. This review aims to examine the animal models expressing myelodysplastic syndrome-associated genes that are currently available and to highlight the most appropriate model to phenocopy myelodysplastic syndrome disease and its risk of transformation to acute myelogenous leukemia. ©2013 Ferrata Storti Foundation. This is an open-access paper. doi:10.3324/haematol.2012.069385 ABSTRACTMouse models myelodysplastic syndrome human candidate genes haematologica | 2013; 98 (1) 11 Figure 1. Mouse models to study malignant hematologic disease. Several strategies can be employed to create mouse models of disease. Candidate genes can be introduced into the germline under the control of appropriate promoters to drive expression in certain cell compartments. Knock-out strategies create gene deficient mice, whilst knock-in strategies use the endogenous promoters; but again these tend to be conditional systems requiring specific promoters to determine in which cell the genes are introduced. Transduction of bone marrow and reinfusion is a powerful tool. Xenograft models are theoretically the best if the techniques involved can be improved.

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SALL4, a novel oncogene, is constitutively expressed in human acute myeloid leukemia (AML) and induces AML in transgenic mice

Abstract: SALL4, a human homolog to Drosophila spalt, is a novel zinc finger transcriptional factor essential for development. We cloned SALL4 and its isoforms (SALL4A and SALL4B).

Cited by 201 publications

References 47 publications

The emerging role of Wnt signaling in the pathogenesis of acute myeloid leukemia

The emerging role of Wnt signaling in the pathogenesis of acute myeloid leukemia

Identification of the nuclear localization signal of SALL4B, a stem cell transcription factor

Engineering mouse models with myelodysplastic syndrome human candidate genes; how relevant are they?

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