Shaoguang Li

ORCID: 0000-0002-8947-9614
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Research Areas
  • Chronic Myeloid Leukemia Treatments
  • Chronic Lymphocytic Leukemia Research
  • Acute Myeloid Leukemia Research
  • Eosinophilic Disorders and Syndromes
  • CAR-T cell therapy research
  • Myeloproliferative Neoplasms: Diagnosis and Treatment
  • Acute Lymphoblastic Leukemia research
  • Cytokine Signaling Pathways and Interactions
  • Lymphoma Diagnosis and Treatment
  • PI3K/AKT/mTOR signaling in cancer
  • Click Chemistry and Applications
  • Cancer-related gene regulation
  • Spine and Intervertebral Disc Pathology
  • T-cell and Retrovirus Studies
  • Cancer, Hypoxia, and Metabolism
  • Integrated Circuits and Semiconductor Failure Analysis
  • Orthopedic Infections and Treatments
  • Fungal Plant Pathogen Control
  • Cell Adhesion Molecules Research
  • Hip and Femur Fractures
  • Bone fractures and treatments
  • Quinazolinone synthesis and applications
  • Fibroblast Growth Factor Research
  • MicroRNA in disease regulation
  • Mast cells and histamine

Chinese PLA General Hospital
2019-2025

University of Massachusetts Chan Medical School
2015-2024

Sun Yat-sen Memorial Hospital
2021-2024

Sun Yat-sen University
2021-2024

Ministry of Natural Resources
2022

Second Affiliated Hospital of Nanchang University
2022

Nanchang University
2022

Ministry of Water Resources of the People's Republic of China
2022

Zhejiang University of Technology
2022

Zhejiang Chinese Medical University
2020

The product of the Philadelphia chromosome (Ph) translocation, BCR/ABL oncogene, exists in three principal forms (P190, P210, and P230 BCR/ABL) that are found distinct Ph-positive leukemia, suggesting proteins have different leukemogenic activity. We directly compared tyrosine kinase activity, vitro transformation properties, vivo activity P190, BCR/ABL. exhibited lower intrinsic than P210 P190. Although all oncogenes transformed both myeloid (32D cl3) lymphoid (Ba/F3) interleukin...

10.1084/jem.189.9.1399 article EN The Journal of Experimental Medicine 1999-05-03

It is generally believed that shutting down the kinase activity of BCR-ABL by imatinib will completely inhibit its functions, leading to inactivation downstream signaling pathways and cure disease. Imatinib highly effective at treating human Philadelphia chromosome-positive (Ph(+)) chronic myeloid leukemia (CML) in phase but not Ph(+) B cell acute lymphoblastic (B-ALL) CML blast crisis. We find SRC kinases activated remain fully active imatinib-treated mouse leukemic cells, suggesting does...

10.1073/pnas.0606509103 article EN Proceedings of the National Academy of Sciences 2006-11-02

Background A somatic activating mutation (V617F) in the JAK2 tyrosine kinase was recently discovered majority of patients with polycythemia vera (PV), and some essential thrombocythemia (ET) chronic idiopathic myelofibrosis. However, role mutant disease pathogenesis is unclear. Methods Findings We expressed murine WT or V617F via retroviral bone marrow transduction/transplantation hematopoietic system two different inbred mouse strains, Balb/c C57Bl/6 (B6). In both V617F, but not WT, induced...

10.1371/journal.pone.0000018 article EN cc-by PLoS ONE 2006-12-20

Constitutive activation of tyrosine kinases, such as the BCR/ABL fusion associated with t(9;22)(q34;q22), is a hallmark chronic myeloid leukemia (CML) syndromes in humans. Expression both necessary and sufficient to cause myeloproliferative syndrome murine bone marrow transplantation models, absolutely depends on kinase activity. Progression CML acute (blast crisis) humans has been acquisition secondary chromosomal translocations, including t(7;11)(p15;p15) resulting NUP98/HOXA9 protein. We...

10.1073/pnas.102583199 article EN Proceedings of the National Academy of Sciences 2002-05-28

A large-scale RNA interference screen reveals a new mechanism of imatinib resistance in chronic myeloid leukemia that can be therapeutically targeted.

10.1126/scitranslmed.3009073 article EN Science Translational Medicine 2014-09-03

Tyrosine kinase inhibitors (TKI) have revolutionized chronic myelogenous leukemia (CML) management. Disease eradication, however, is hampered by innate resistance of leukemia-initiating cells (LIC) to TKI-induced killing, which also provides the basis for subsequent emergence TKI-resistant mutants. We report that EZH2, catalytic subunit Polycomb Repressive Complex 2 (PRC2), overexpressed in CML LICs and required colony formation survival cell-cycle progression cell lines. A critical role...

10.1158/2159-8290.cd-15-1439 article EN Cancer Discovery 2016-09-15

Abstract Diagnostic histopathology is a gold standard for diagnosing hematopoietic malignancies. Pathologic diagnosis requires labor-intensive reading of large number tissue slides with high diagnostic accuracy equal or close to 100 percent guide treatment options, but this requirement difficult meet. Although artificial intelligence (AI) helps reduce the labor pathologic slides, has not reached clinically usable level. Establishment an AI model often demands big datasets and ability handle...

10.1038/s41467-020-19817-3 article EN cc-by Nature Communications 2020-11-26

Although alveolar epithelial type II cells (AECII) perform substantial roles in the maintenance of integrity, extent their contributions to immune defense is poorly understood. Here, we demonstrate that AECII activates macrophages (AM) functions, such as phagocytosis using a conditioned medium from infected by P. aeruginosa. AECII-derived chemokine MCP-1, monocyte chemoattractant protein, was identified main factor enhancing AM function. We proposed enhanced potency may play critical role...

10.1371/journal.pone.0004891 article EN cc-by PLoS ONE 2009-03-20

Cancer stem cells (CSCs) are responsible for the initiation and maintenance of some types cancer, suggesting that inhibition these may limit disease progression relapse. Unfortunately, few CSC-specific genes have been identified. Here, we determined gene encoding arachidonate 15-lipoxygenase (Alox15/15-LO) is essential survival leukemia (LSCs) in a murine model BCR-ABL-induced chronic myeloid (CML). In absence Alox15, BCR-ABL was unable to induce CML mice. Furthermore, Alox15 deletion...

10.1172/jci66129 article EN Journal of Clinical Investigation 2014-08-07

Although skeletal progenitors provide a reservoir for bone-forming osteoblasts, the major energy source their osteogenesis remains unclear. Here, we demonstrate requirement mitochondrial oxidative phosphorylation in osteogenic commitment and differentiation of progenitors. Deletion Evolutionarily Conserved Signaling Intermediate Toll pathways (ECSIT) hinders bone formation regeneration, resulting deformity, defects marrow niche spontaneous fractures followed by persistent nonunion. Upon...

10.1038/s41467-022-34694-8 article EN cc-by Nature Communications 2022-11-11

Osteomyelitis is a major challenge in global healthcare, as it requires the simultaneous management of bone defects and bacterial infections, which poses considerable difficulties for orthopedic clinicians. In this study, we developed berberine liposome-modified cement specifically aimed at treating osteomyelitis induced by Staphylococcus aureus. We characterized physical properties modified cement, conducted vitro antibacterial assays to evaluate its efficacy eradicating aureus biofilm,...

10.1021/acsomega.4c11198 article EN cc-by-nc-nd ACS Omega 2025-02-12
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