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  • S. Karger AG  (8)
  • 2015-2019  (8)
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  • S. Karger AG  (8)
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  • 2015-2019  (8)
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  • 1
    Online Resource
    Online Resource
    Guidelines for Diagnosis and Treatment of Primary Liver Cancer in China (2017 Edition)
    S. Karger AG ; 2018
    In:  Liver Cancer Vol. 7, No. 3 ( 2018), p. 235-260
    Details
    In: Liver Cancer, S. Karger AG, Vol. 7, No. 3 ( 2018), p. 235-260
    Abstract: 〈 b 〉 〈 i 〉 Background: 〈 /i 〉 〈 /b 〉 Hepatocellular carcinoma (HCC) (about 85–90% of primary liver cancer) is particularly prevalent in China because of the high prevalence of chronic hepatitis B infection. HCC is the fourth most common malignancy and the third leading cause of tumor-related deaths in China. It poses a significant threat to the life and health of Chinese people. 〈 b 〉 〈 i 〉 Summary: 〈 /i 〉 〈 /b 〉 This guideline presents official recommendations of the National Health and Family Planning Commission of the People’s Republic of China on the surveillance, diagnosis, staging, and treatment of HCC occurring in China. The guideline was written by more than 50 experts in the field of HCC in China (including liver surgeons, medical oncologists, hepatologists, interventional radiologists, and diagnostic radiologists) on the basis of recent evidence and expert opinions, balance of benefits and harms, cost-benefit strategies, and other clinical considerations. 〈 b 〉 〈 i 〉 Key Messages: 〈 /i 〉 〈 /b 〉 The guideline presents the Chinese staging system, and recommendations regarding patients with HCC in China to ensure optimum patient outcomes.
    Type of Medium: Online Resource
    ISSN: 2235-1795 , 1664-5553
    URL: Article
    DOI: 10.1159/000488035
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2018
    detail.hit.zdb_id: 2666925-0
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  • 2
    Online Resource
    Online Resource
    Predictive Capabilities of Three Widely Used Pathology Classification Systems and a Simplified Classification (Beijing Classification) in Primary IgA Nephropathy
    S. Karger AG ; 2019
    In:  Kidney and Blood Pressure Research Vol. 44, No. 5 ( 2019), p. 928-941
    Details
    In: Kidney and Blood Pressure Research, S. Karger AG, Vol. 44, No. 5 ( 2019), p. 928-941
    Abstract: 〈 b 〉 〈 i 〉 Background/Aims: 〈 /i 〉 〈 /b 〉 Several pathological classification systems were commonly used in clinical practice to predict the prognosis of IgA nephropathy (IgAN). However, how prognostic value differs between these systems is unclear. The aim of this study was to compare the Lee grade, the Oxford classification, and the Haas classification and to find a simplified classification. 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 We retrospectively analyzed IgAN cases diagnosed between January 2002 and December 2007. The endpoints were progression to end-stage renal disease (ESRD) or a ≥50% decline in estimated glomerular filtration rate (eGFR). The predictive capabilities were evaluated by comparing the ability of discrimination (continuous net reclassification) and calibration (Akaike information criterion [AIC]). 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 A total of 412 IgAN patients were included in the study. The average follow-up period was 80.62 ± 23.63 months. A total of 44 (10.68%) patients progressed to ESRD, and 70 (16.99%) patients showed a ≥50% decline in eGFR. All multivariate Cox regression models had limited power for high AIC values. The prognostic values of the Lee grade and the Oxford classification were higher than those of models containing only established baseline clinical indicators for progression to ESRD or a ≥50% decline in eGFR (Lee grade 0.50, 95% CI 0.21–0.74; Oxford classification 0.48, 95% CI 0.28–0.71). The prognostic value of the Haas classification was lower than that of the other pathological classification systems for progression to ESRD or a ≥50% decline in eGFR (Lee grade 0.53, 95% CI 0.23–0.92; Oxford classification 0.59, 95% CI 0.10–0.74). The prognostic value of hierarchical classification (Beijing classification) using M and T lesion was similar to the Oxford classification. 〈 b 〉 〈 i 〉 Conclusions: 〈 /i 〉 〈 /b 〉 Both the Lee grade and the Oxford classification showed incremental prognostic values beyond established baseline clinical indicators. The Haas classification was slightly inferior to the Lee grade and the Oxford classification. The hierarchical classification (Beijing classification) using less pathological parameters does not lose predictive efficiency.
    Type of Medium: Online Resource
    ISSN: 1420-4096 , 1423-0143
    URL: Article
    DOI: 10.1159/000500459
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2019
    detail.hit.zdb_id: 1482922-8
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    Online Resource
  • 3
    Online Resource
    Online Resource
    MYBL2 is a Potential Prognostic Marker that Promotes Cell Proliferation in Gallbladder Cancer
    S. Karger AG ; 2017
    In:  Cellular Physiology and Biochemistry Vol. 41, No. 5 ( 2017), p. 2117-2131
    Details
    In: Cellular Physiology and Biochemistry, S. Karger AG, Vol. 41, No. 5 ( 2017), p. 2117-2131
    Abstract: Background: Gallbladder cancer (GBC) is an aggressive and highly lethal biliary tract malignancy, with extremely poor prognosis. In the present study, we analyzed the potential involvement of MYBL2, a member of the Myb transcription factor family, in the carcinogenesis of human GBC. Methods: MYBL2 expression levels were measured in GBC and cholecystitis tissue specimens using quantitative real-time PCR (qRT-PCR) and immunohistochemical (IHC) assays. The effects of MYBL2 on cell proliferation and DNA synthesis were evaluated using Cell Counting Kit-8 assay (CCK-8), colony formation, and 5-ethynyl-2'-deoxyuridine (EdU) retention assay, flow cytometry analysis, western blot, and a xenograft model of GBC cells in nude mice. Results: MYBL2 expression was increased in GBC tissues and associated with histological differentiation, tumour invasion, clinical stage and unfavourable overall survival in GBC patients. The downregulation of MYBL2 expression resulted in the inhibition of GBC cell proliferation, and DNA replication in vitro, and the growth of xenografted tumours in nude mice. Conversely, MYBL2 overexpression resulted in the opposite effects. Conclusions: MYBL2 overexpression promotes GBC cell proliferation through the regulation of the cell cycle at the S and G2/M phase transitions. Thus, MYBL2 could serve as a potential prognostic and therapeutic biomarker in GBC patients.
    Type of Medium: Online Resource
    ISSN: 1015-8987 , 1421-9778
    URL: Article
    DOI: 10.1159/000475454
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2017
    detail.hit.zdb_id: 1482056-0
    SSG: 12
    SSG: 15,3
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    Online Resource
  • 4
    Online Resource
    Online Resource
    Isocitrate Dehydrogenase 2 Suppresses the Invasion of Hepatocellular Carcinoma Cells via Matrix Metalloproteinase 9
    S. Karger AG ; 2015
    In:  Cellular Physiology and Biochemistry Vol. 37, No. 6 ( 2015), p. 2405-2414
    Details
    In: Cellular Physiology and Biochemistry, S. Karger AG, Vol. 37, No. 6 ( 2015), p. 2405-2414
    Abstract: Background/Aims: Isocitrate dehydrogenase 2 (IDH2) is a mitochondrial NADP-dependent isocitrate dehydrogenase, and has been found to be a tumor suppressor in several types of tumors. However, the roles of IDH2 in hepatocellular carcinoma (HCC) as well as underlying mechanisms remain unknown. Methods: The IDH2 and matrix metalloproteinase 9 (MMP9) levels in the specimens from 24 HCC patients were investigated by Western blot and ELISA, respectively. Their relationship was examined by correlation analyses. Patient survival with high IDH2 levels and low IDH2 levels was compared. IDH2 levels and MMP9 levels were modified in a human HCC cell line. The effects of IDH2 or MMP9 modulation on the expression of the other were analyzed. The effects of IDH2 on cell invasion were analyzed in a transwell cell invasion assay. The dependence of nuclear factor κB (NF-κB) signaling was examined using a specific inhibitor. Results: The IDH2 levels significantly decreased in HCC, and were lower in HCC with metastases, compared to those without metastases. IDH2 levels inversely correlated with MMP9 levels in HCC. HCC patients with Low IDH2 had lower 5-year survival. MMP9 levels did not regulate IDH2 levels, while IDH2 inhibited MMP9 levels in HCC cells, in a NF-κB signaling dependent manner, possibly through iκB, to suppress HCC cell invasion. Conclusions: Down regulation of IDH2 may promote HCC cell invasion via NF-κB-dependent increases in MMP9 activity. IDH2 may be a potential therapeutic target for HCC.
    Type of Medium: Online Resource
    ISSN: 1015-8987 , 1421-9778
    URL: Article
    DOI: 10.1159/000438593
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2015
    detail.hit.zdb_id: 1482056-0
    SSG: 12
    SSG: 15,3
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  • 5
    Online Resource
    Online Resource
    High Prevalence of HBV Lamivudine-Resistant Mutations in HBV/HIV Co-Infected Patients on Antiretroviral Therapy in the Area with the Highest Prevalence of HIV/HBV Co-Infection in China
    S. Karger AG ; 2018
    In:  Intervirology Vol. 61, No. 3 ( 2018), p. 123-132
    Details
    In: Intervirology, S. Karger AG, Vol. 61, No. 3 ( 2018), p. 123-132
    Abstract: 〈 b 〉 〈 i 〉 Objectives: 〈 /i 〉 〈 /b 〉 We aimed to determine the prevalence of hepatitis B virus (HBV) drug-resistant mutations in patients co- infected with HBV/human immunodeficiency virus (HIV), including both drug-naïve subjects and those who received antiretroviral therapy (ART) in Guangxi, where the prevalence of HIV/HBV co-infection is highest in China. 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 Two hundred and three subjects co-infected with HBV/HIV were recruited, including 123 drug-naïve patients (group 1) and 80 who received ART (group 2). The polymerase gene of HBV in the serum of all study subjects was analysed. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 The results showed that the prevalence of HBV drug-resistant mutations in group 2 (76.5%, 95% CI 56.3–96.7) was significantly higher than that in group 1 (1.4%, 95% CI –1.4 to 4.2; χ 〈 sup 〉 2 〈 /sup 〉 = 50.955, 〈 i 〉 p 〈 /i 〉 & #x3c; 0.05). The major pattern of lamivudine (3TC)-resistant mutations is L180M+M204I+L80I (35.7%). In total, 95% of subjects with resistant mutations had cross-resistance to telbivudine and entecavir. No putative tenofovir disoproxil fumarate (TDF) resistance change was found. Five subjects (6.5%) in group 2 had HBV viral loads over 10 × 10 〈 sup 〉 6 〈 /sup 〉 copies/mL. Four of them had 3TC-resistant mutations. Multivariate analysis showed that ART was the only factor associated with the development of drug-resistant mutations. 〈 b 〉 〈 i 〉 Conclusion: 〈 /i 〉 〈 /b 〉 Treating HIV in HIV/HBV co-infection with antiretroviral agents may result in a very high prevalence of HBV 3TC-resistant mutations. TDF could not completely suppress HBV replication.
    Type of Medium: Online Resource
    ISSN: 0300-5526 , 1423-0100
    URL: Article
    DOI: 10.1159/000493797
    RVK:
    XA 10000
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2018
    detail.hit.zdb_id: 1482863-7
    SSG: 12
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  • 6
    Online Resource
    Online Resource
    Role of the TGFβ/PDCD4/AP-1 Signaling Pathway in Nasopharyngeal Carcinoma and Its Relationship to Prognosis
    S. Karger AG ; 2017
    In:  Cellular Physiology and Biochemistry Vol. 43, No. 4 ( 2017), p. 1392-1401
    Details
    In: Cellular Physiology and Biochemistry, S. Karger AG, Vol. 43, No. 4 ( 2017), p. 1392-1401
    Abstract: Background: The objective of the present study was to evaluate the role of the TGFβ/PDCD4/AP-1 pathway in nasopharyngeal carcinoma (NPC) and its relationship to NPC prognosis. Methods: NPC tissues collected from 66 NPC patients were compared to 17 nasopharyngeal mucosa biopsy specimens collected as normal tissues. Immunohistochemical staining was performed to assess expression of transforming growth factor-β receptor I (TGFβRI), programmed cell death 4 (PDCD4) and activator protein-1 (AP-1). The Kaplan-Meier method was applied to evaluate NPC patient overall survival (OS) and progression-free-survival (PFS). Cox regression analysis was used to estimate independent prognostic factors for NPC. The human NPC cell line CNE2 was selected and treated with SB431542, an inhibitor of TGFβRI; expression of TGFβRI and PDCD4 in CNE2 cells was determined by western blotting. NPC tissues showed higher expression of TGFβRI and AP-1 but lower expression of PDCD4 than normal tissues (all P 〈 0.05). Results: The results of Kaplan-Meier analysis showed that TGFβRI-positive patients and AP-1-positive patients had shorter OS and PFS than TGFβRI-negative patients and AP-1-negative patients; additionally, PDCD4-positive patients had higher OS and PFS than PDCD4-negative patients. Cox regression analysis revealed that advanced tumor stage, overexpression of TGFβRI and AP-1, and low expression of PDCD4 were unfavorable factors influencing OS and PFS in NPC patients. Compared with the control group, expression of TGFβRI decreased and that of PDCD4 increased significantly in CNE2 cells treated with the inhibitor (all P 〈 0.05). These findings indicate that the TGFβ/PDCD4/AP-1 pathway may be associated with NPC development and progression. Conclusion: High expression of TGFβRI and AP-1 and low expression of PDCD4 may be unfavorable prognostic factors for NPC.
    Type of Medium: Online Resource
    ISSN: 1015-8987 , 1421-9778
    URL: Article
    DOI: 10.1159/000481871
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2017
    detail.hit.zdb_id: 1482056-0
    SSG: 12
    SSG: 15,3
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    Online Resource
  • 7
    Online Resource
    Online Resource
    Aquaporin-3 Inhibition Reduces the Growth of NSCLC Cells Induced by Hypoxia
    S. Karger AG ; 2016
    In:  Cellular Physiology and Biochemistry Vol. 38, No. 1 ( 2016), p. 129-140
    Details
    In: Cellular Physiology and Biochemistry, S. Karger AG, Vol. 38, No. 1 ( 2016), p. 129-140
    Abstract: Background/Aims: Non-small cell lung cancer (NSCLC) is the leading cause of death worldwide. Although aquaporin-3 (AQP3) is widely distributed in mammalian tissues and over-expressed in NSCLC cells, there are limited studies on the effects of AQP3 knockdown on NSCLC cells under hypoxic conditions. Methods: The CCK-8 assay was used to calculate cell viability. Scratch-wound healing and transwell assays were used to detect cell migration and invasion. Apoptotic cells were measured by the TUNEL assay. mRNA expression levels were calculated via quantitative RT-PCR. Relative protein levels were determined by immunoblot assays. Results: AQP3 knockdown substantially reduced proliferation, migration, and invasion of A549 and NCI-H460 cells under hypoxic conditions. Moreover, AQP3 knockdown clearly induced cell apoptosis. Further analysis identified levels of HIF-1α, VEGF, Raf, phosphor-MEK, and phosphor-ERK, whose activities were significantly attenuated in the AQP3 knockdown group. Conclusions: These findings indicate that AQP3 knockdown retards the growth of NSCLC cells partially through inhibiting HIF-1α/VEGF and Raf/MEK/ERK signalling pathways.
    Type of Medium: Online Resource
    ISSN: 1015-8987 , 1421-9778
    URL: Article
    DOI: 10.1159/000438615
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2016
    detail.hit.zdb_id: 1482056-0
    SSG: 12
    SSG: 15,3
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  • 8
    Online Resource
    Online Resource
    Activation of Peroxisome Proliferator-Activated Receptor γ (PPARγ) Through NF-κB/Brg1 and TGF-ß1 Pathways Attenuates Cardiac Remodeling in Pressure-Overloaded Rat Hearts
    S. Karger AG ; 2015
    In:  Cellular Physiology and Biochemistry Vol. 35, No. 3 ( 2015), p. 899-912
    Details
    In: Cellular Physiology and Biochemistry, S. Karger AG, Vol. 35, No. 3 ( 2015), p. 899-912
    Abstract: Background/Aims: Cardiac remodeling is a common pathophysiological change along with chronic hypertension and myocardial infarction. Recent evidence indicated that cardiac tissue expressed peroxisome proliferator-activated receptor γ (PPARγ). However, the functional role of PPARγ in cardiac remodeling remained unclear. The present study was designed to investigate the relationship between PPARγ activation and pressure overload-induced cardiac remodeling. Methods: Cardiac remodeling model was successfully established by abdominal aorta ligation. Cardiac fibrosis and cardiomyocyte hypertrophy were simulated by 100 nM angiotensin II (Ang II) in vitro. Haemodynamic parameters, the expressions of Brg1, a-MHC, ß-MHC, transforming growth factor beta 1 (TGF-ß1), collagen-I, collagen-III and NF-γB were examined. Results: Morphological and haemodynamic measurements showed that the activation of PPARγ improved the impaired cardiac function and decreased interstitial fibrosis in cardiac remodeling rats. Further results also showed that the activation of PPARγ inhibited the expressions of Brg1 and TGF-ß1 in the cardiac remodeling hearts. The activation of PPARγ also inhibited the proliferation and collagen production of cardiac fibroblasts, and down-regulated the activity of Brg1 and the expression of TGF-ß1 induced by Ang II in cultured neonatal rat cardiomyocytes and cardiac fibroblasts, respectively, through NF-γB pathway. Conclusions: These results suggested that PPARγ activation effectively inhibited cardiac remodeling processes by suppression of Brg1 and TGF-ß1 expressions through NF-γB pathway in the pressure-overloaded hearts induced by abdominal aorta ligation in rats.
    Type of Medium: Online Resource
    ISSN: 1015-8987 , 1421-9778
    URL: Article
    DOI: 10.1159/000369747
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2015
    detail.hit.zdb_id: 1482056-0
    SSG: 12
    SSG: 15,3
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