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Lingyun Wu

Researcher at Shanghai Jiao Tong University

Publications -  88
Citations -  1446

Lingyun Wu is an academic researcher from Shanghai Jiao Tong University. The author has contributed to research in topics: Decitabine & Myelodysplastic syndromes. The author has an hindex of 19, co-authored 75 publications receiving 1034 citations. Previous affiliations of Lingyun Wu include University of Nebraska Medical Center & Cincinnati Children's Hospital Medical Center.

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Journal ArticleDOI

Tumor-Associated Neutrophils in Cancer: Going Pro.

TL;DR: This review summarizes the most recent updates regarding neutrophil recruitments and functions in the tumor microenvironment as well as potential development of neutrophils-targeted putative therapeutic strategies.
Journal ArticleDOI

Overexpression of the EZH2, RING1 and BMI1 genes is common in myelodysplastic syndromes: relation to adverse epigenetic alteration and poor prognostic scoring.

TL;DR: Excessive overexpression of the EZH2, RING1, and BMI1 genes is common in MDS and indicate poor prognosis, as well as the relationship between the expression of PcG genes and epigenetic alteration and prognosis-risk scoring, which is explored for the first time.
Journal ArticleDOI

Iron overload promotes mitochondrial fragmentation in mesenchymal stromal cells from myelodysplastic syndrome patients through activation of the AMPK/MFF/Drp1 pathway.

TL;DR: The iron chelation or antioxidant weakened the activity of the AMPK/MFF/Drp1 pathway in MDS-MSCs with IO from several patients, accompanied by attenuation of mitochondrial fragmentation and autophagy.
Journal ArticleDOI

TP53 mutations predict decitabine-induced complete responses in patients with myelodysplastic syndromes.

TL;DR: TP53 mutations might predict decitabine‐induced complete responses in patients with MDS, and DAC‐induced responses may result from partial suppression of malignant clones containing mutated TP53 genes.
Book ChapterDOI

Neutrophils in the Tumor Microenvironment.

TL;DR: This chapter will discuss the phenotypic and functional changes in the neutrophil in the tumor microenvironment, the underlying mechanism(s) of neutrophic facilitated cancer metastasis, and clinical potential of neutrophils as a prognostic/diagnostic marker and therapeutic target.