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  • S. Karger AG  (16)
  • Medicine  (16)
  • 1
    In: Oncology, S. Karger AG, Vol. 98, No. 3 ( 2020), p. 186-194
    Abstract: 〈 b 〉 〈 i 〉 Background: 〈 /i 〉 〈 /b 〉 The clinical course of hepatocellular carcinoma (HCC) is complicated, because it often recurs and shows multiple lesions, some of which progress to a more malignant form, shortening the life of the patient. The hepatocyte growth factor receptor c-Met has been shown to play an important role in the pathogenesis of HCC, but the influence of c-Met expression on the clinical course of HCC remains to be fully elucidated. 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 We randomly selected and included 600 tumor specimens obtained from the primary and recurrent lesions of 319 HCC cases between 1995 and 2007. The expression of c-Met was determined by immunohistochemistry using archived formalin-fixed paraffin-embedded samples. We analyzed the correlation between c-Met expression and clinical parameters, including survival. In addition, we examined c-Met expression in the malignant transition of HCC in all cases including recurrent lesions. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 Survival analysis using the multivariate Cox proportional-regression model revealed that the prognosis was significantly better in the primary cases with high c-Met expression than in those with low c-Met expression (hazard ratio 0.159, 95% confidence interval 0.065–0.391; 〈 i 〉 p 〈 /i 〉 & #x3c; 0.001). During the course of recurrence, some cases with high c-Met expression returned to low c-Met expression. Among 40 cases with high c-Met expression, 29 survived more than 2 years after detecting the high c-Met expression. 〈 b 〉 〈 i 〉 Conclusion: 〈 /i 〉 〈 /b 〉 High expression of c-Met may be a prognostic factor for a good, rather than a poor, HCC prognosis. The involvement of c-Met expression in the malignant transition of recurrent HCC is obscure.
    Type of Medium: Online Resource
    ISSN: 0030-2414 , 1423-0232
    RVK:
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2020
    detail.hit.zdb_id: 1483096-6
    detail.hit.zdb_id: 250101-6
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  • 2
    Online Resource
    Online Resource
    S. Karger AG ; 2006
    In:  Intervirology Vol. 49, No. 1-2 ( 2006), p. 51-57
    In: Intervirology, S. Karger AG, Vol. 49, No. 1-2 ( 2006), p. 51-57
    Abstract: Although hepatitis C virus (HCV) targets the liver, it has become increasingly evident that HCV can induce diseases of many organs. Recently, much attention is drawn to metabolic disorders in HCV infection. First, hepatic steatosis and derangement in lipid metabolism have been found characteristic of HCV infection, and later on, a correlation was noted between HCV infection and diabetes as well as insulin resistance. We have demonstrated that HCV by itself can induce insulin resistance through disturbing the insulin signaling pathway by HCV proteins. The fact that HCV infection induces insulin resistance by the virus itself may influence the progression of chronic liver disease and open up novel therapeutic approaches. In conclusion, towards the future, HCV infection needs to be viewed not only as a liver disease but also as a metabolic disease.
    Type of Medium: Online Resource
    ISSN: 0300-5526 , 1423-0100
    RVK:
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2006
    detail.hit.zdb_id: 1482863-7
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    S. Karger AG ; 2010
    In:  Oncology Vol. 78, No. Suppl. 1 ( 2010), p. 24-30
    In: Oncology, S. Karger AG, Vol. 78, No. Suppl. 1 ( 2010), p. 24-30
    Abstract: Persistent infection with hepatitis C virus (HCV) is a major risk toward development of hepatocellular carcinoma. A number of transgenic mouse lines carrying the cDNA of HCV genome have been established and evaluated in the study of HCV pathogenesis. Among those, the studies using transgenic mouse lines that carry the HCV genome containing the core gene indicate the direct involvement of HCV in pathogenicity, including that in oncogenesis. Oxidative stress overproduction and intracellular signaling augmentation are shown to be the key events in HCV-associated hepatocarcinogenesis. Besides the data in hepatitis C patients, connecting liver fibrosis progression and the disturbance in lipid and glucose metabolisms, these mouse models also show a close relationship between HCV and metabolic alterations including hepatic steatosis and insulin resistance. Furthermore, the persistent activation of peroxisome proliferator-activated receptor-α has recently been found, yielding dramatic changes in the lipid metabolism and oxidative stress overproduction in cooperation with the mitochondrial dysfunction. These results would provide a clue for further understanding of the role of lipid metabolism in pathogenesis of hepatitis C including liver injury and hepatocarcinogenesis.
    Type of Medium: Online Resource
    ISSN: 0030-2414 , 1423-0232
    RVK:
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2010
    detail.hit.zdb_id: 1483096-6
    detail.hit.zdb_id: 250101-6
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  • 4
    In: Digestion, S. Karger AG, Vol. 103, No. 5 ( 2022), p. 367-377
    Abstract: 〈 b 〉 〈 i 〉 Background/Aims: 〈 /i 〉 〈 /b 〉 Although most patients with presumptive colonic diverticular bleeding (CDB) do not undergo a small bowel investigation in clinical practice, no prospective study supports this management. We evaluated the utility of early small bowel capsule endoscopy (CE) after negative colonoscopy results. 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 This prospective study evaluated the diagnostic yield of early small bowel CE (≤3 days from visit) for consecutive patients with acute-onset hematochezia, when colonoscopy found colonic diverticulosis but did not identify the definite bleeding source ( 〈 i 〉 n 〈 /i 〉 = 51; presumptive CDB). As a matched control for comparing clinical outcomes, presumptive CDB patients without CE ( 〈 i 〉 n 〈 /i 〉 = 51) were retrospectively extracted. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 On CE for the prospective cohort, the rates of total positive findings, P2 findings (high bleeding potential according to the P classification), and blood pooling in the colon were 57%, 12% (ulceration, 8%; angioectasia, 4%), and 24%, respectively. The rates of rebleeding within 30 and 365 days were 16% and 29% in the prospective cohort with CE, respectively, and were not significantly different from those in the retrospective cohort without CE (10% and 25%, respectively). In addition, thromboembolism and mortality within 30 and 365 days were not significantly different between those with and without CE. 〈 b 〉 〈 i 〉 Conclusion: 〈 /i 〉 〈 /b 〉 Early CE detected a suspected small bowel bleeding source in 12% of acute-onset presumptive CDB patients but did not significantly improve major clinical outcomes. Therefore, routine CE is unnecessary for presumptive CDB patients after colonoscopy (UMIN000026676).
    Type of Medium: Online Resource
    ISSN: 0012-2823 , 1421-9867
    RVK:
    RVK:
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2022
    detail.hit.zdb_id: 1482218-0
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  • 5
    In: Digestion, S. Karger AG
    Abstract: Introduction: Submucosal invasion is a core hallmark of early gastric cancer (EGC) with poor prognosis. However, the molecular mechanism of the progression from intramucosal gastric cancer (IMGC) to early submucosal-invasive gastric cancer (SMGC) is not fully understood. The objective of this study was to identify genes and pathways involved in the submucosal invasion in EGC using comprehensive gene expression analysis. Methods: Gene expression profiling was performed for eight cases of IMGC and eight cases of early SMGC with submucosal invasion ≥500 μm. To validate the findings of gene expression analysis and to examine the gene expression pattern in tissues, immunohistochemical (IHC) staining was performed for 50 cases of IMGC and SMGC each. Results: Gene expression analysis demonstrated that the expression levels of small intestine-specific genes were significantly decreased in SMGC. Among them, defensin alpha 5 (DEFA5) was the most downregulated gene in SMGC, which was further validated in SMGC tissues by IHC staining. Gene set enrichment analysis showed a strong association between SMGC, the JAK-STAT signaling pathway, and the upregulation of STAT3-activating cytokines. The expression of phosphorylated STAT3 was significant in the nucleus of tumor cells in SMGC tissues but not in areas expressing DEFA5. Conclusion: The results of this study strongly suggest that the downregulation of DEFA5 and the activation of STAT3 play a significant role in the submucosal invasion of EGC.
    Type of Medium: Online Resource
    ISSN: 0012-2823 , 1421-9867
    RVK:
    RVK:
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2023
    detail.hit.zdb_id: 1482218-0
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  • 6
    Online Resource
    Online Resource
    S. Karger AG ; 1995
    In:  Intervirology Vol. 38, No. 3-4 ( 1995), p. 134-142
    In: Intervirology, S. Karger AG, Vol. 38, No. 3-4 ( 1995), p. 134-142
    Type of Medium: Online Resource
    ISSN: 0300-5526 , 1423-0100
    RVK:
    Language: English
    Publisher: S. Karger AG
    Publication Date: 1995
    detail.hit.zdb_id: 1482863-7
    SSG: 12
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  • 7
    In: Digestion, S. Karger AG, Vol. 102, No. 6 ( 2021), p. 903-910
    Abstract: 〈 b 〉 〈 i 〉 Background: 〈 /i 〉 〈 /b 〉 The diagnostic clues for autoimmune gastritis (AIG) can be classified into 2 categories: endoscopic findings and pathological diagnosis. We believe that research on the AIG detection rate by endoscopists could provide a better understanding of the diagnosis of AIG. This study aimed to clarify the ratio of the endoscopic and the pathological diagnoses of AIG. 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 We retrospectively reviewed consecutive patients who underwent esophagogastroduodenoscopy (EGD). During their first EGD, the gastric mucosa with C2 atrophy or more was biopsied for pathological evaluation based on the updated Sydney system. A gastric biopsy was also performed after 〈 i 〉 Helicobacter pylori 〈 /i 〉 eradication, obtaining specimens from at least 2 sites, the greater curvature of the corpus and the antrum. We enrolled patients who were positive for the anti-parietal cell antibody and were diagnosed with AIG, histologically and/or endoscopically. The detection rates of AIG were compared between endoscopic diagnosis and pathological diagnosis. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 A total of 10,822 patients underwent EGD during the study period. Finally, 41 patients with AIG were enrolled, leading to an AIG prevalence of 0.38% in this study. As for the clue leading to AIG detection, 31.7% (13/41) were diagnosed through endoscopy (proximal-predominant atrophy), and 68.3% (28/41) were diagnosed pathologically. The AIG detection rate by endoscopists in the posteradication group was significantly lower than in 〈 i 〉 the H. pylori-negative 〈 /i 〉 group ( 〈 i 〉 p 〈 /i 〉 & #x3c; 0.05). 〈 b 〉 〈 i 〉 Conclusion: 〈 /i 〉 〈 /b 〉 Endoscopists frequently overlooked AIG, especially in posteradication cases. Pathological assessment using the updated Sydney system after 〈 i 〉 H. pylori 〈 /i 〉 eradication might be a promising strategy to detect AIG better.
    Type of Medium: Online Resource
    ISSN: 0012-2823 , 1421-9867
    RVK:
    RVK:
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2021
    detail.hit.zdb_id: 1482218-0
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  • 8
    In: Oncology, S. Karger AG, Vol. 80, No. 1-2 ( 2011), p. 97-101
    Abstract: 〈 i 〉 Objective: 〈 /i 〉 The aim of this study was to investigate the effect of gemcitabine and oxaliplatin combination chemotherapy on refractory pancreatic cancer. 〈 i 〉 Methods: 〈 /i 〉 Patients with advanced pancreatic cancer refractory to gemcitabine and S-1 were treated with gemcitabine 1,000 mg/m 〈 sup 〉 2 〈 /sup 〉 over 30 min and oxaliplatin 85 mg/m 〈 sup 〉 2 〈 /sup 〉 over 120 min on days 1 and 15. Treatment was repeated every 4 weeks and tumor response was assessed every two cycles by RECIST version 1.0. 〈 i 〉 Results: 〈 /i 〉 Twenty-two patients with pathologically confirmed pancreatic cancer were enrolled. The treatment was administered as a second-line chemotherapy in eighteen patients (82%) and as a third-line chemotherapy in four patients (18%). Tumor response did not occur in any of the cases. Thirteen patients demonstrated stable diseases, and the disease control rate was 59%. Median overall survival and time to progression were 6.8 months (95% CI, 2.8–11.5) and 2.6 months (95% CI, 1.5–3.8), respectively. Median overall survival from the first-line chemotherapy was 22.7 months (95% CI, 14.8–24.4). The major grade 3/4 adverse events included neutropenia (14%), anorexia (23%), and peripheral neuropathy (14%). 〈 i 〉 Conclusions: 〈 /i 〉 Gemcitabine and oxaliplatin combination chemotherapy was tolerable but had limited activity in patients with advanced pancreatic cancer in a refractory setting.
    Type of Medium: Online Resource
    ISSN: 0030-2414 , 1423-0232
    RVK:
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2011
    detail.hit.zdb_id: 1483096-6
    detail.hit.zdb_id: 250101-6
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  • 9
    In: Oncology, S. Karger AG, Vol. 85, No. 5 ( 2013), p. 269-277
    Abstract: 〈 b 〉 〈 i 〉 Objectives: 〈 /i 〉 〈 /b 〉 Elevated plasma fibrinogen levels are associated with tumor progression and poor outcomes in cancer patients. We investigated the prognostic value of pretreatment plasma fibrinogen levels in patients with hepatocellular carcinoma (HCC). 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 One hundred and thirteen patients with newly diagnosed HCC were retrospectively evaluated. We investigated the correlation between pretreatment plasma fibrinogen levels, clinicopathological parameters and overall survival. Both univariate and multivariate analyses were performed to identify the clinicopathological parameters associated with overall survival. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 The median value of the pretreatment plasma fibrinogen level was 279 mg/dl. Elevated plasma fibrinogen levels were associated with larger tumor size, the presence of vascular invasion and higher Cancer Liver Italian Program scores. Lower plasma fibrinogen levels were associated with higher Child-Pugh grades. The overall survival rates in patients with pretreatment plasma fibrinogen levels ≥315 mg/dl were significantly lower than those with a pretreatment plasma fibrinogen level 〈 315 mg/dl (p = 0.016). On multivariate analysis, the plasma fibrinogen levels (per 100 mg/dl) were found to be independently associated with overall survival (hazard ratio 1.236; p = 0.046). 〈 b 〉 〈 i 〉 Conclusions: 〈 /i 〉 〈 /b 〉 This study demonstrates that elevated pretreatment plasma fibrinogen levels are associated with tumor progression and are independently associated with a poor prognosis in patients with HCC.
    Type of Medium: Online Resource
    ISSN: 0030-2414 , 1423-0232
    RVK:
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2013
    detail.hit.zdb_id: 1483096-6
    detail.hit.zdb_id: 250101-6
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  • 10
    Online Resource
    Online Resource
    S. Karger AG ; 2002
    In:  Oncology Vol. 62, No. Suppl. 1 ( 2002), p. 29-37
    In: Oncology, S. Karger AG, Vol. 62, No. Suppl. 1 ( 2002), p. 29-37
    Type of Medium: Online Resource
    ISSN: 1423-0232 , 0030-2414
    RVK:
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2002
    detail.hit.zdb_id: 1483096-6
    detail.hit.zdb_id: 250101-6
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