Yi-Yang Chen

ORCID: 0000-0002-7675-0129
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About
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Research Areas
  • Acute Myeloid Leukemia Research
  • Myeloproliferative Neoplasms: Diagnosis and Treatment
  • Chronic Lymphocytic Leukemia Research
  • Lymphoma Diagnosis and Treatment
  • Viral-associated cancers and disorders
  • Kruppel-like factors research
  • Protein Degradation and Inhibitors
  • Lung Cancer Research Studies
  • Platelet Disorders and Treatments
  • Multiple Myeloma Research and Treatments
  • Head and Neck Cancer Studies
  • Ubiquitin and proteasome pathways
  • Hematological disorders and diagnostics
  • Glioma Diagnosis and Treatment
  • Cytokine Signaling Pathways and Interactions
  • Histone Deacetylase Inhibitors Research
  • Antiplatelet Therapy and Cardiovascular Diseases
  • Neutropenia and Cancer Infections
  • Blood groups and transfusion
  • Hematopoietic Stem Cell Transplantation

Chiayi Chang Gung Memorial Hospital
2015-2021

University of Duisburg-Essen
2020

Essen University Hospital
2020

Memorial Hospital of South Bend
2013

Acute myeloid leukemia (AML) is characterized by a high relapse rate and dismal long-term overall survival which related to persistence of leukemia-initiating cells in their niche. Different animal models malignancies reveal how neoplastic alter the structural functional characteristics hematopoietic stem cell niche reinforce malignancy. Understanding disruption microenvironmental interactions with AML are vital need. Malignant niches frequently go along inflammatory responses, but impact on...

10.1182/bloodadvances.2019001292 article EN cc-by-nc-nd Blood Advances 2020-07-02

Abstract Murine models of myeloid neoplasia show how leukemia infiltration alters the hematopoietic stem cell (HSC) niche to reinforce malignancy at expense healthy hematopoiesis. However, little is known about bone marrow architecture in humans and its impact on clinical outcome. Here, we dissect patients with acute (AML) first diagnosis. We combined immunohistochemical stainings global gene expression analyses from these AML correlated them features. Mesenchymal progenitor cells (MSPCs)...

10.1182/bloodadvances.2020001808 article EN cc-by-nc-nd Blood Advances 2020-10-27

High mobility group AT-hook 2 (HMGA2) is an architectural transcription factor that negatively regulated by let-7 microRNA through binding to it's 3′-untranslated region. Transgenic mice expressing Hmga2 with a truncation of its region has been shown exhibit myeloproliferative phenotype. To decipher the let-7-HMGA2 axis in neoplasms, we employed vitro model supplemented clinical correlation. Ba/F3 cells inducible JAK2V617F expression (Ton.JAK2.V617F cells) showed upregulation HMGA2...

10.3324/haematol.2016.154385 article EN cc-by-nc Haematologica 2017-01-05

Myelofibrosis (MF) is a pathologic entity of myeloproliferative neoplasm (MPN) characterized by bone marrow fibrosis, extramedullary hematopoiesis, splenomegaly, and constitutional symptoms that severely affect the quality life accompanied with risk leukemia development. Conventional treatment usually ineffective has limited impact on prolongation survival. Dysregulated Janus kinase (JAK) signaling common in MPN. In two randomized controlled trials, ruxolitinib, potent pan-JAK inhibitor,...

10.1179/1607845415y.0000000036 article EN Hematology 2015-07-27

Complex and multiple mechanisms are involved in the etiology of Hepatitis C virus-associated immune thrombocytopenia (HCV-ITP). Many hematopoietic growth factors affect thrombopoiesis. The aim this study was to clarify interaction thrombopoietic patients with HCV-ITP.We selected 33 HCV-ITP 17 normal individuals. We compare serum interleukin (IL)-3, IL-6, IL-11, thrombopoietin (Tpo), stem cell factor (SCF), granulocyte-macrophage colony-stimulating (GM-CSF), tumour necrosis factor-α (TNFα),...

10.1080/10245332.2016.1204493 article EN Hematology 2016-07-09

Phenotypic heterogeneity and molecular diversity make diffuse large B-cell lymphoma (DLBCL) a challenging disease. We recently illustrated that amoeboid movement plays an indispensable role in DLBCL dissemination inadvertently identified the inhibitor of bromodomain extra-terminal (BET) proteins JQ1 could repress migration. To explore further, we dissected impacts BET inhibition DLBCL. found abrogated cells through both restraining RAS signaling suppressing MYC-mediated RhoA activity. also...

10.3390/cancers13195024 article EN Cancers 2021-10-07
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