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Journal Article 4

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hematopoiesis 4

leukemia 2

21) 1

in vivo imaging 1

AML1-ETO 1

CD34+ 1

Kasumi-1 1

MyD88 1

TGF-β 1

TLR 1

Zfyve16 1

bone marrow failure 1

endofin 1

hematopoietic stem cell 1

lymphocytes 1

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mutation 1

myelodysplastic syndrome 1

pathway hits 1

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In vivo imaging of hematopoietic stem cell development in the zebrafish

Panpan Zhang, Feng Liu

Frontiers of Medicine 2011, Volume 5, Issue 3, Pages 239-247 doi: 10.1007/s11684-011-0123-0

Abstract: The zebrafish is an excellent model for imaging of hematopoiesis due to its transparent embryo at early

Keywords： hematopoietic stem cell hematopoiesis in vivo imaging transgenics zebrafish

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Toll-like receptor signaling in hematopoietic homeostasis and the pathogenesis of hematologic diseases

Joseph Cannova,Peter Breslin S.J.,Jiwang Zhang

Frontiers of Medicine 2015, Volume 9, Issue 3, Pages 288-303 doi: 10.1007/s11684-015-0412-0

Abstract: Accumulating evidence suggests that TLR signaling is involved in normal hematopoiesis and specific hematologicthe molecular mechanisms by which TLR signaling mediates the regulation of both normal and pathogenic hematopoiesis

Keywords： TLR MyD88 hematopoiesis bone marrow failure leukemia myelodysplastic syndrome

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AML1-ETO driven acute leukemia: insights into pathogenesis and potential therapeutic approaches

Megan A. Hatlen, Lan Wang, Stephen D. Nimer

Frontiers of Medicine 2012, Volume 6, Issue 3, Pages 248-262 doi: 10.1007/s11684-012-0206-6

Abstract:

The AML1-ETO fusion transcription factor is generated by the t(8;21) translocation, which is present in approximately 4%–12% of adult and 12%–30% of pediatric acute myeloid leukemia (AML) patients. Both human and mouse models of AML have demonstrated that AML1-ETO is insufficient for leukemogenesis in the absence of secondary events. In this review, we discuss the pathogenetic insights that have been gained from identifying the various events that can cooperate with AML1-ETO to induce AML in vivo. We also discuss potential therapeutic strategies for t(8;21) positive AML that involve targeting the fusion protein itself, the proteins that bind to it, or the genes that it regulates. Recently published studies suggest that a targeted therapy for t(8;21) positive AML is feasible and may be coming sometime soon.

Keywords： AML1-ETO mouse model leukemia t(8 21) pathway hits mutation hematopoiesis Kasumi-1 CD34+

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Zfyve16 regulates the proliferation of B-lymphoid cells

Xuemei Zhao, Donghe Li, Qingsong Qiu, Bo Jiao, Ruihong Zhang, Ping Liu, Ruibao Ren

Frontiers of Medicine 2018, Volume 12, Issue 5, Pages 559-565 doi: 10.1007/s11684-017-0562-3

Abstract:

Zfyve16 (a.k.a. endofin or endosome-associated FYVE-domain protein), a member of the FYVE-domain protein family, is involved in endosomal trafficking and in TGF-β, BMP, and EGFR signaling. The FYVE protein SARA regulates the TGF-β signaling pathway by recruiting Smad2/3 and accelerating their phosphorylation, thereby altering their susceptibility to TGF-β-mediated T cell suppression. Zfyve16 binds to Smad4 and their binding affects the formation of Smad2/3-Smad4 complex in TGF-β signaling. However, the in vivo function of Zfyve16 remains unknown. In this study, we generated a Zfyve16 knockout mouse strain (Zfyve16^KO) and examined its hematopoietic phenotypes and hematopoietic reconstruction ability. The proportion of T cells in the peripheral blood of Zfyve16^KO mice increases compared with that in wild-type mice. This finding is consistent with the role of Zfyve16 in facilitating TGF-β signaling. Unpredictably, B cell proliferation is inhibited in Zfyve16^KO mice. The proliferation potential of Zfyve16^KO B-lymphoid cells also significantly decreases in vitro. These results suggest that Zfyve16 inhibits the proliferation of T cells, possibly through the TGF-β signaling, but upregulates the proliferation of B-lymphoid cells.