Bin Zhang

ORCID: 0000-0003-4703-7524
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Research Areas
  • Acute Myeloid Leukemia Research
  • Chronic Myeloid Leukemia Treatments
  • MicroRNA in disease regulation
  • Chronic Lymphocytic Leukemia Research
  • RNA modifications and cancer
  • Cancer-related molecular mechanisms research
  • Immune Cell Function and Interaction
  • CAR-T cell therapy research
  • Acute Lymphoblastic Leukemia research
  • Cancer-related gene regulation
  • Hematopoietic Stem Cell Transplantation
  • Epigenetics and DNA Methylation
  • RNA Research and Splicing
  • RNA Interference and Gene Delivery
  • Circular RNAs in diseases
  • Eosinophilic Disorders and Syndromes
  • Myeloproliferative Neoplasms: Diagnosis and Treatment
  • Histone Deacetylase Inhibitors Research
  • Immune cells in cancer
  • Protein Degradation and Inhibitors
  • Blood Coagulation and Thrombosis Mechanisms
  • Hemophilia Treatment and Research
  • Platelet Disorders and Treatments
  • HER2/EGFR in Cancer Research
  • Cancer, Hypoxia, and Metabolism

City of Hope
2016-2025

Beckman Research Institute
2015-2025

City Of Hope National Medical Center
2014-2025

Guangdong Provincial Hospital of Traditional Chinese Medicine
2025

Guangzhou University of Chinese Medicine
2025

Chinese PLA General Hospital
2021-2025

Henan University of Science and Technology
2024

Institute of Hematology & Blood Diseases Hospital
2023

Chinese Academy of Medical Sciences & Peking Union Medical College
2023

The Ohio State University
2023

We characterized leukemia stem cells (LSC) in chronic phase myelogenous (CML) using a transgenic mouse model. LSC were restricted to with long-term hematopoietic cell (LTHSC) phenotype. CML LTHSC demonstrated reduced homing and retention the bone marrow (BM), related decreased CXCL12 expression BM, resulting from increased G-CSF production by cells. Altered cytokine BM was associated selective impairment of normal growth advantage LTHSC. Imatinib (IM) treatment partially corrected...

10.1016/j.ccr.2012.02.018 article EN publisher-specific-oa Cancer Cell 2012-04-01

The success of tyrosine kinase inhibitors (TKIs) in treating chronic myeloid leukemia (CML) depends on the requirement for BCR-ABL1 activity CML progenitors. However, quiescent HSCs are TKI resistant and represent a kinase-independent disease reservoir. Here we have shown that persistence leukemic BM requires inhibition tumor suppressor protein phosphatase 2A (PP2A) expression--but not activity--of oncogene. Examination from patients healthy individuals revealed PP2A was suppressed compared...

10.1172/jci68951 article EN Journal of Clinical Investigation 2013-09-02

Abstract INTRODUCTION With the advancement of disease‐modifying therapies for Alzheimer's disease (AD), validating plasma biomarkers against cerebrospinal fluid (CSF) and positron emission tomography (PET) standards is crucial in both research real‐world settings. METHODS We measured phosphorylated tau (p‐tau)217, p‐tau181, amyloid beta (Aβ)1‐40, Aβ1‐42, neurofilament light chain cohorts. Participants were categorized by brain status using US Food Drug Administration/European Medicines...

10.1002/alz.14536 article EN cc-by Alzheimer s & Dementia 2025-01-30

Mutations in LMAN1 (ERGIC-53) and MCFD2 are thecauses of a human genetic disorder, combined deficiency coagulation factorV factor VIII. is type 1 transmembrane protein with homology tomannose-binding lectins. soluble EF-hand-containing that isretained the endoplasmic reticulum through its interaction LMAN1. Weshowed endogenous present primarily complex witheach other 1:1 stoichiometry, although not required foroligomerization Using cross-linking-immunoprecipitation assay, wedetected specific...

10.1074/jbc.m502160200 article EN cc-by Journal of Biological Chemistry 2005-05-11

Targeting the Hedgehog (Hh) pathway represents a potential leukaemia stem cell (LSC)-directed therapy which may compliment tyrosine kinase inhibitors (TKIs) to eradicate LSC in chronic phase (CP) myeloid (CML). We set out elucidate role of Hh signaling CP-CML and determine if inhibition signaling, through smoothened (SMO), was an effective strategy target LSC. Assessment gene protein expression demonstrated that is activated CD34(+) stem/progenitor cells. LDE225 (Sonidegib), small molecule,...

10.1038/srep25476 article EN cc-by Scientific Reports 2016-05-09

Abstract Induction of reactive oxygen species (ROS), an important process for the cytotoxicity various acute myeloid leukemia (AML) therapies including hypomethylating agents (HMAs), concurrently activates NF‐E2‐related factor 2 (Nrf2) antioxidant response pathway which in turn results induction enzymes that neutralize ROS. In this study, we demonstrated Nrf2 inhibition is additional mechanism responsible marked antileukemic activity AML seen with combination HMAs and venetoclax (ABT‐199)....

10.1002/jcp.28091 article EN Journal of Cellular Physiology 2019-01-08

The mechanisms responsible for cervical cancer radioresistance are still largely unexplored. present study aimed to identify miRNAs associated with of cells.The radioresistant cell variants were established by repeated selection irradiation. miRNA profiles cells and their corresponding controls analyzed compared using microarray. Differentially expressed confirmed quantitative real-time PCR. Cervical transfected miRNA-specific mimics or inhibitors. Radiosensitivity determined colony-forming...

10.1186/1475-2867-13-118 article EN cc-by Cancer Cell International 2013-11-27
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