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  1. Article ; Online: Current Status and Prospects of Clinical Treatment of Osteosarcoma.

    Jiang, Zong-Yuan / Liu, Ji-Bin / Wang, Xiao-Feng / Ma, Yu-Shui / Fu, Da

    Technology in cancer research & treatment

    2022  Volume 21, Page(s) 15330338221124696

    Abstract: Osteosarcoma, one of the common malignant tumors in the skeletal system, originates in mesenchymal tissue, and the most susceptible area of occurrence is the metaphysis with its abundant blood supply. Tumors are characterized by highly malignant spindle ... ...

    Abstract Osteosarcoma, one of the common malignant tumors in the skeletal system, originates in mesenchymal tissue, and the most susceptible area of occurrence is the metaphysis with its abundant blood supply. Tumors are characterized by highly malignant spindle stromal cells that can produce bone-like tissue. Most of the osteosarcoma are primary, and a few are secondary. Osteosarcoma occurs primarily in children and adolescents undergoing vigorous bone growth and development. Most cases involve rapid tumor development and early blood metastasis. In recent years, research has grown in the areas of molecular biology, imaging medicine, biological materials, applied anatomy, surgical techniques, biomechanics, and comprehensive treatment of tumors. With developments in molecular biology and tissue bioengineering, treatment methods have also made great progress, especially in comprehensive limb salvage treatment, which significantly enhances the quality of life after surgery and improves the 5-year survival rate of patients with malignant tumors. This article provides a review of limb salvage, immunotherapy, gene therapy, and targeted therapy from traditional amputation to neoadjuvant chemotherapy, providing a reference for current clinical treatments for osteosarcoma.
    MeSH term(s) Adolescent ; Biological Products/therapeutic use ; Bone Neoplasms/diagnosis ; Bone Neoplasms/pathology ; Bone Neoplasms/therapy ; Child ; Humans ; Limb Salvage ; Osteosarcoma/drug therapy ; Osteosarcoma/therapy ; Quality of Life
    Chemical Substances Biological Products
    Language English
    Publishing date 2022-10-11
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 2146365-7
    ISSN 1533-0338 ; 1533-0346
    ISSN (online) 1533-0338
    ISSN 1533-0346
    DOI 10.1177/15330338221124696
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5871: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  2. Article: Nonoxid-HMGB1 Attenuates Cognitive Impairment After Traumatic Brain Injury in Rats.

    Chen, Jun-Quan / Gao, Shuang-Qi / Luo, Lun / Jiang, Zong-Yuan / Liang, Chao-Feng / He, Hai-Yong / Guo, Ying

    Frontiers in medicine

    2022  Volume 9, Page(s) 827585

    Abstract: Traumatic brain injury (TBI) is a major global burden of health. As an accepted inflammatory mediator, high mobility group box 1 (HMGB1) is found to be effective in facilitating neurogenesis and axonal regeneration. SH3RF2 (also known as POSHER), an E3 ... ...

    Abstract Traumatic brain injury (TBI) is a major global burden of health. As an accepted inflammatory mediator, high mobility group box 1 (HMGB1) is found to be effective in facilitating neurogenesis and axonal regeneration. SH3RF2 (also known as POSHER), an E3 ligase SH3 domain-containing ring finger 2, belongs to the SH3RF family of proteins. Here, we aimed to investigate the role of redox states of HMGB1 on neurite outgrowth and regeneration both
    Language English
    Publishing date 2022-04-11
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2775999-4
    ISSN 2296-858X
    ISSN 2296-858X
    DOI 10.3389/fmed.2022.827585
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Treatment with b-AP15 to Inhibit UCHL5 and USP14 Deubiquitinating Activity and Enhance p27 and Cyclin E1 for Tumors with

    Jiang, Zong-Yuan / Hong, Jiang / Zhang, Ju-Hua / Wang, Xiao-Feng / Ma, Yu-Shui / Xiong, Zhang-Xia / Sun, Hao-Ran / Cheng, Cong / Xie, Bang-Zhu / Liu, Ji-Bin / Ouyang, Yang-Gang / Fu, Da

    Technology in cancer research & treatment

    2022  Volume 21, Page(s) 15330338221119745

    Abstract: Background: ...

    Abstract Background:
    MeSH term(s) Animals ; Cell Line, Tumor ; Humans ; Mice ; Piperidones/pharmacology ; Proteasome Endopeptidase Complex/genetics ; Proteasome Endopeptidase Complex/metabolism ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism ; Ubiquitin Thiolesterase/genetics ; Ubiquitin Thiolesterase/metabolism ; Ubiquitination
    Chemical Substances Piperidones ; Tumor Suppressor Protein p53 ; USP14 protein, human ; Usp14 protein, mouse ; UCHL5 protein, human (EC 3.4.19.12) ; Ubiquitin Thiolesterase (EC 3.4.19.12) ; Proteasome Endopeptidase Complex (EC 3.4.25.1)
    Language English
    Publishing date 2022-08-16
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2146365-7
    ISSN 1533-0338 ; 1533-0346
    ISSN (online) 1533-0338
    ISSN 1533-0346
    DOI 10.1177/15330338221119745
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5871: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  4. Article ; Online: Inhibition of USP14 and UCH37 deubiquitinating activity by b-AP15 as a potential therapy for tumors with p53 deficiency.

    Ma, Yu-Shui / Wang, Xiao-Feng / Yu, Fei / Wu, Ting-Miao / Liu, Ji-Bin / Zhang, Yun-Jie / Xia, Qing / Jiang, Zong-Yuan / Lin, Qin-Lu / Fu, Da

    Signal transduction and targeted therapy

    2020  Volume 5, Issue 1, Page(s) 30

    MeSH term(s) Animals ; Disease Models, Animal ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Lymphoma/drug therapy ; Lymphoma/genetics ; Lymphoma/pathology ; Piperidones/pharmacology ; Tumor Suppressor Protein p53/deficiency ; Tumor Suppressor Protein p53/genetics ; Ubiquitin Thiolesterase/genetics
    Chemical Substances 3,5-bis((4-nitrophenyl)methylidene)-1-prop-2-enoylpiperidin-4-one ; Piperidones ; Trp53 protein, mouse ; Tumor Suppressor Protein p53 ; Usp14 protein, mouse ; Ubiquitin Thiolesterase (EC 3.4.19.12) ; Uchl5 protein, mouse (EC 3.4.19.12)
    Language English
    Publishing date 2020-04-01
    Publishing country England
    Document type Letter ; Research Support, Non-U.S. Gov't
    ZDB-ID 2886872-9
    ISSN 2059-3635 ; 2095-9907
    ISSN (online) 2059-3635
    ISSN 2095-9907
    DOI 10.1038/s41392-020-0143-9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Downregulation of miR-223 and miR-19a induces differentiation and promotes recruitment of osteoclast cells in giant-cell tumor of the bone via the Runx2/TWIST-RANK/RANKL pathway.

    Jiang, Zong-Yuan / Jiang, Jun-Jian / Ma, Yu-Shui / Li, Hong-Ye / Shi, Wei / Fu, Pei-Liang / Xu, Cong-Feng / Lu, Jiu-Zhou / Fu, Da / Xu, Jian-Guang

    Biochemical and biophysical research communications

    2018  Volume 505, Issue 4, Page(s) 1003–1009

    Abstract: Giant-cell tumor (GCT) of the bone is an invasiveness and high recurrent bone tumor that is considered borderline or potentially malignant. To explore the molecular mechanism leading to bone destruction and identify novel targets for treatment, we ... ...

    Abstract Giant-cell tumor (GCT) of the bone is an invasiveness and high recurrent bone tumor that is considered borderline or potentially malignant. To explore the molecular mechanism leading to bone destruction and identify novel targets for treatment, we conducted silencing of miR-223 and miR-19a in stromal giant cells and identified TWIST and Runx2 as their target genes. We investigated the impact of these microRNAs and their target genes on stromal giant cells that promote the differentiation of monocyte/macrophages into osteoclast cells and recruitment to the bone microenvironment, which in turn enhances the bone destruction capacity of GCT. MiR-223 and miR-19a were found to regulate the expression of TWIST and Runx2, influence the RANKL-RANK pathway and the expression of MCP-1, and finally regulate the pathophysiological process of osteolytic bone destruction. Our results indicate that re-expression of miR-223 and miR-19a induces an inhibitory effect on the bone destruction capacity of GCT, suggesting that re-expression of miR-223 and miR-19a can be a novel strategy for the treatment of GCT.
    MeSH term(s) Bone Neoplasms/metabolism ; Bone Neoplasms/pathology ; Cell Differentiation ; Core Binding Factor Alpha 1 Subunit/genetics ; Core Binding Factor Alpha 1 Subunit/metabolism ; Down-Regulation ; Giant Cell Tumor of Bone/metabolism ; Giant Cell Tumor of Bone/pathology ; Humans ; MicroRNAs/metabolism ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Osteoclasts/metabolism ; Osteoclasts/pathology ; RANK Ligand/genetics ; RANK Ligand/metabolism ; Receptor Activator of Nuclear Factor-kappa B/genetics ; Receptor Activator of Nuclear Factor-kappa B/metabolism ; Tumor Cells, Cultured ; Twist-Related Protein 1/genetics ; Twist-Related Protein 1/metabolism
    Chemical Substances Core Binding Factor Alpha 1 Subunit ; MIRN19 microRNA, human ; MIRN223 microRNA, human ; MicroRNAs ; Nuclear Proteins ; RANK Ligand ; RUNX2 protein, human ; Receptor Activator of Nuclear Factor-kappa B ; TNFRSF11A protein, human ; TNFSF11 protein, human ; TWIST1 protein, human ; Twist-Related Protein 1
    Language English
    Publishing date 2018-10-09
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 205723-2
    ISSN 1090-2104 ; 0006-291X ; 0006-291X
    ISSN (online) 1090-2104 ; 0006-291X
    ISSN 0006-291X
    DOI 10.1016/j.bbrc.2018.10.025
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 116: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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