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  1. Article ; Online: Bronchiolar adenoma in the right upper lobe of the lung: A case report.

    Xia, Liqin

    Asian journal of surgery

    2023  Volume 46, Issue 9, Page(s) 4090–4091

    MeSH term(s) Humans ; Lung ; Lung Neoplasms ; Adenoma
    Language English
    Publishing date 2023-04-25
    Publishing country Netherlands
    Document type Case Reports ; Letter
    ZDB-ID 1068461-x
    ISSN 0219-3108 ; 1015-9584
    ISSN (online) 0219-3108
    ISSN 1015-9584
    DOI 10.1016/j.asjsur.2023.04.069
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Invasive cribriform carcinoma of the breast: A case report.

    Xia, Liqin / Chen, Xiao

    Asian journal of surgery

    2022  Volume 46, Issue 2, Page(s) 1130–1131

    MeSH term(s) Humans ; Female ; Adenocarcinoma/pathology ; Carcinoma ; Breast/pathology ; Breast Neoplasms/diagnostic imaging ; Breast Neoplasms/surgery ; Prognosis
    Language English
    Publishing date 2022-08-20
    Publishing country China
    Document type Case Reports ; Letter
    ZDB-ID 1068461-x
    ISSN 0219-3108 ; 1015-9584
    ISSN (online) 0219-3108
    ISSN 1015-9584
    DOI 10.1016/j.asjsur.2022.08.012
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Oncogenic miR-20b-5p contributes to malignant behaviors of breast cancer stem cells by bidirectionally regulating CCND1 and E2F1.

    Xia, Liqin / Li, Feng / Qiu, Jun / Feng, Zhongming / Xu, Zihan / Chen, Zhengtang / Sun, Jianguo

    BMC cancer

    2020  Volume 20, Issue 1, Page(s) 949

    Abstract: Background: Breast cancer is the leading cause of cancer mortality in women worldwide. Therefore, it is of great significance to identify the biological mechanism of tumorigenesis and explore the development of breast cancer to achieve a better ... ...

    Abstract Background: Breast cancer is the leading cause of cancer mortality in women worldwide. Therefore, it is of great significance to identify the biological mechanism of tumorigenesis and explore the development of breast cancer to achieve a better prognosis for individuals suffering from breast cancer. MicroRNAs (miRNAs) have become a hot topic in cancer research, but the underlying mechanism of its involvement in cancer remains unclear.
    Methods: The miRNA profile between breast cancer stem cells (BCSCs, CD44
    Results: MiR-20b-5p had the highest degree in both the miRNA-gene network and miRNA-GO network to regulate BCSCs. Overexpression of miR-20b-5p significantly promoted the migration and wound healing ability of MCF-7 cells and T47D cells compared with the control (P < 0.05). In addition, miR-20b-5p facilitated the proliferation of MCF-7 cells and T47D-CSCs (P < 0.05) and inhibited the apoptosis of T47D-CSCs (P < 0.05). Moreover, miR-20b-5p promoted xenograft growth compared with the control group (P < 0.05). Accordingly, potential targets of both CCND1 and E2F1 were predicted by bioinformatics analysis. MiR-20b-5p directly targeted both CCND1 and E2F1 in a dual luciferase assay, while antagomir-20b-5p downregulated the protein levels of CCND1 and E2F1.
    Conclusions: Oncogenic miR-20b-5p was confirmed to promote the malignant behaviors of breast cancer cells and BCSCs. The underlying mechanism lies in that miR-20b-5p overall enhanced both CCND1 and E2F1 targets via bidirectional regulation probably involving direct downregulation and indirect upregulation.
    MeSH term(s) Animals ; Breast Neoplasms/genetics ; Cell Proliferation ; Cyclin D1/metabolism ; E2F1 Transcription Factor/metabolism ; Female ; Humans ; Mice ; Mice, Nude ; Neoplastic Stem Cells/metabolism ; Oncogenes/genetics ; Transfection
    Chemical Substances CCND1 protein, human ; E2F1 Transcription Factor ; E2F1 protein, human ; Cyclin D1 (136601-57-5)
    Language English
    Publishing date 2020-10-02
    Publishing country England
    Document type Journal Article
    ISSN 1471-2407
    ISSN (online) 1471-2407
    DOI 10.1186/s12885-020-07395-y
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Phosphatase and tensin homolog deleted on chromosome 10 degradation induced by NEDD4 promotes acquired erlotinib resistance in non-small-cell lung cancer.

    Sun, Huake / Ma, Huiwen / Wang, Jianmin / Xia, Liqin / Zhu, Guangkuo / Wang, Zhoufei / Sun, Jianguo / Chen, Zhengtang

    Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine

    2017  Volume 39, Issue 7, Page(s) 1010428317709639

    Abstract: Acquired resistance to epidermal growth factor receptor-tyrosine kinase inhibitors, such as gefitinib and erlotinib, is a critical issue in the treatment of patients with epidermal growth factor receptor mutant-positive non-small-cell lung cancer. Recent ...

    Abstract Acquired resistance to epidermal growth factor receptor-tyrosine kinase inhibitors, such as gefitinib and erlotinib, is a critical issue in the treatment of patients with epidermal growth factor receptor mutant-positive non-small-cell lung cancer. Recent evidence suggests that downregulation of gene of phosphatase and tensin homolog deleted on chromosome 10 plays an important role in acquired resistance to epidermal growth factor receptor-tyrosine kinase inhibitors in various types of cancers, including lung cancer. It was reported that the E3 ubiquitin ligase neural precursor cell expressed developmentally downregulated gene (NEDD4) (also known as NEDD4-1) negatively regulated phosphatase and tensin homolog deleted on chromosome 10 protein levels through poly-ubiquitination and proteolysis in carcinomas of the prostate, lung, and bladder. Whether this process plays a role in epidermal growth factor receptor-tyrosine kinase inhibitors resistance in non-small-cell lung cancer has not been studied extensively. In view of this, we investigated the involvement of NEDD4 and phosphatase and tensin homolog deleted on chromosome 10 in acquired erlotinib resistance with tyrosine kinase inhibitor-sensitive (HCC827) or tyrosine kinase inhibitor-resistant (Erlotinib-resistant HCC827/ER cells which harbored exon 19 deletion. Overexpression of NEDD4 in HCC827/ER cells was detected, and the reverse correlation between NEDD4 and phosphatase and tensin homolog deleted on chromosome 10 expression in these cells was also revealed. In HCC827/ER cells with knockdown of NEDD4, phosphatase and tensin homolog deleted on chromosome 10 and p-Akt expressions were decreased; the sensitivity of HCC827/ER cells to erlotinib was partially restored. Similar results were also observed in vivo. In H1650/ER cells harboring both exon 19 and phosphatase and tensin homolog deleted on chromosome 10 deletion, expression of p-Akt and sensitivity to erlotinib were not affected by simple knockdown of NEDD4 but affected after transfection of phosphatase and tensin homolog deleted on chromosome 10 into H1650/ER cells. Our results demonstrate that NEDD4 may promote the acquired resistance of non-small-cell lung cancer cells to erlotinib by decreasing phosphatase and tensin homolog deleted on chromosome 10 protein expression. Targeted decrease in NEDD4 expression may be a potential therapeutic strategy for tyrosine kinase inhibitor-resistant non-small-cell lung cancer.
    MeSH term(s) Apoptosis/drug effects ; Carcinoma, Non-Small-Cell Lung/drug therapy ; Carcinoma, Non-Small-Cell Lung/genetics ; Carcinoma, Non-Small-Cell Lung/pathology ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Drug Resistance, Neoplasm/genetics ; Endosomal Sorting Complexes Required for Transport/genetics ; Erlotinib Hydrochloride/administration & dosage ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Mutation ; Nedd4 Ubiquitin Protein Ligases ; PTEN Phosphohydrolase/genetics ; Signal Transduction ; Ubiquitin-Protein Ligases/genetics ; Xenograft Model Antitumor Assays
    Chemical Substances Endosomal Sorting Complexes Required for Transport ; Erlotinib Hydrochloride (DA87705X9K) ; Nedd4 Ubiquitin Protein Ligases (EC 2.3.2.26) ; Nedd4 protein, human (EC 2.3.2.26) ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; PTEN Phosphohydrolase (EC 3.1.3.67) ; PTEN protein, human (EC 3.1.3.67)
    Language English
    Publishing date 2017-07
    Publishing country United States
    Document type Journal Article
    ZDB-ID 605825-5
    ISSN 1423-0380 ; 0289-5447 ; 1010-4283
    ISSN (online) 1423-0380
    ISSN 0289-5447 ; 1010-4283
    DOI 10.1177/1010428317709639
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1598: Show issues Location:
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  5. Article ; Online: Clinical benefit from EGFR-TKI plus ginsenoside Rg3 in patients with advanced non-small cell lung cancer harboring EGFR active mutation.

    Li, Yan / Wang, Yanmei / Niu, Kai / Chen, Xiewan / Xia, Liqin / Lu, Dingxi / Kong, Rui / Chen, Zhengtang / Duan, Yuzhong / Sun, Jianguo

    Oncotarget

    2016  Volume 7, Issue 43, Page(s) 70535–70545

    Abstract: Purpose: Acquired resistance is a bottleneck that restricts the efficacy of epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) for lung cancer. Ginsenoside Rg3 is an antiangiogenic agent which can down-regulate the expressions of ... ...

    Abstract Purpose: Acquired resistance is a bottleneck that restricts the efficacy of epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) for lung cancer. Ginsenoside Rg3 is an antiangiogenic agent which can down-regulate the expressions of vascular endothelial growth factor (VEGF) and EGFR. Combination of EGFR-TKI and ginsenoside Rg3 may be a promising strategy to delay acquired resistance. This retrospective study explored the efficacy and safety of this combined regimen in patients with EGFR mutation and advanced non-small cell lung cancer (NSCLC).
    Results: By the deadline of March 31th 2016, the median follow-up period reached 22.9 months. The median PFS was significantly longer in group A than in group B (12.4 months vs 9.9 months, P = 0.017). In addition, ORR was significantly higher in group A than in group B (59.6% vs 41.7%, P = 0.049). The median OS in group A showed no extended tendency compared with that in group B (25.4 months vs 21.4 months, P = 0.258). No significant difference in side effects was found between the two groups.
    Methods: A total of 124 patients with advanced NSCLC and EGFR active mutation were collected and analyzed. All of them were treated with first-line EGFR-TKI and divided into two groups. In group A (n=52), patients were administered EGFR-TKI plus ginsenoside Rg3 at standard doses. In group B (n=72), patients received EGFR-TKI alone. Progression-free survival (PFS), overall survival (OS), objective response rate (ORR) and side effects were analyzed.
    Conclusions: Ginsenoside Rg3 improves median PFS and ORR of first-line EGFR-TKI treatment in EGFR-mutant advanced NSCLC patients, thus providing a new regimen to delay acquired resistance of EGFR-TKI.
    Language English
    Publishing date 2016-10-25
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2560162-3
    ISSN 1949-2553 ; 1949-2553
    ISSN (online) 1949-2553
    ISSN 1949-2553
    DOI 10.18632/oncotarget.12059
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: [Image analysis of deformation of occluding device before and after the occlusion of PDA with Amplatzer].

    Zhou, Tong-fu / Hua, Yi-min / Liu, Han-min / Xia, Li-qin / Wang, Ze-rong / Jin, Zhong-he

    Zhonghua er ke za zhi = Chinese journal of pediatrics

    2003  Volume 41, Issue 5, Page(s) 371–373

    MeSH term(s) Adolescent ; Blood Vessel Prosthesis Implantation ; Child ; Child, Preschool ; Ductus Arteriosus, Patent/therapy ; Equipment and Supplies ; Female ; Humans ; Infant ; Male ; Video Recording
    Language Chinese
    Publishing date 2003-05
    Publishing country China
    Document type Journal Article
    ZDB-ID 784523-6
    ISSN 0578-1310
    ISSN 0578-1310
    Database MEDical Literature Analysis and Retrieval System OnLINE

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