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| 1 | Deacetylase inhibitors-focus on non-histone targets and effects显示文摘Inhibitors of protein deacetylases have recently been established as a novel therapeutic principle for several human diseases,including cancer.The original notion of the mechanism of action of these compounds focused on the epigenetic control of transcriptional processes, especially of tumor suppressor genes,by interfering with the acetylation status of nuclear histone proteins,hence the name histone deacetylase inhibitors was coined.Yet,this view could not explain the high specificity for tumor cells and recent evidence now suggests that non-histone proteins represent major targets for protein deacetylase inhibitors and that the post-translational modification of the acetylome is involved in various cellular processes of differentiation,survival and cell death induction. | Matthias Ocker | 2010 | World Journal of Biological Chemistry2010，1，5： | 11 |
| 2 | Improvement of quantitative testing of liver function in patients with chronic hepatitis C after installment of antiviral therapy显示文摘AIM: To investigate if and to what extent antiviral therapy influenced a broad panel of quantitative testing of liver function (QTLF).METHODS: Fifty patients with chronic hepatitis C were either treated with interferon (n = 8), interferon/ribavirin (n = 19) or peg-interferon/ribavirin (n = 23). Quantitative testing of liver function, including aminopyrine breath test (ABT), galactose elimination capacity (GEC), sorbitol clearance (SCI) and indocyanine green clearance (ICG)was performed before and 3 mo after initiation of antiviral therapy.RESULTS: After 3 mo of antiviral treatment, 36 patients showed normal transaminases and were negative for HCV-RNA, 14 patients did not respond to therapy. ABT and GEC as parameters of microsomal and cytosolic liver function were reduced in all patients before therapy initiation and returned to normal values in the 36 therapy responders after 3 mo. Parameters of liver perfusion (SCI and ICG) were not affected by antiviral therapy. In the 14 non-responders,no changes in QTLF values were observed during the treatment period.CONCLUSION: ICG and SCI remained unaffected in patients with chronic hepatitis C, while ABT and GEC were significantly compromised. ABT and GEC normalized in responders to antiviral therapy. Early determination of ABT and GEC may differentiate responders from non-responders to antivJral treatment in hepatitis C. | Matthias Ocker Marion Ganslmayer Steffen Zopf Susanne Gahr Christopher Janson Eckhart G. Hahn Christoph Herold | 2005 | World Journal of Gastroenterology2005，11，35： | 8 |
| 3 | Epigenetics and pancreatic cancer:Pathophysiology and novel treatment aspects显示文摘An improvement in pancreatic cancer treatment represents an urgent medical goal.Late diagnosis and high intrinsic resistance to conventional chemotherapy has led to a dismal overall prognosis that has remained unchanged during the past decades.Increasing knowledge about the molecular pathogenesis of the disease has shown that genetic alterations,such as mutations of K-ras,and especially epigenetic dysregulation of tumor-associated genes,such as silencing of the tumor suppressor p16ink4a,are hallmarks of pancreatic cancer.Here,we describe genes that are commonly affected by epigenetic dysregulation in pancreatic cancer via DNA methylation,histone acetylation or miRNA(microRNA)expression,and review the implications on pancreatic cancer biology such as epithelial-mesenchymal transition,morphological pattern formation,or cancer stem cell regulation during carcinogenesis from PanIN(pancreatic intraepithelial lesions)to invasive cancer and resistance development.Epigenetic drugs,such as DNA methyltransferases or histone deactylase inhibitors,have shown promising preclinical results in pancreatic cancer and are currently in early phases of clinical development.Combinations of epigenetic drugs with established cytotoxic drugs or targeted therapies are promising approaches to improve the poor response and survival rate of pancreatic cancer patients. | Daniel Neureiter Tarkan Jger Matthias Ocker Tobias Kiesslich | 2014 | World Journal of Gastroenterology2014，20，24： | 6 |
| 4 | Fibroblast growth factor signaling in non-alcoholic fatty liver disease and non-alcoholic steatohepatitis:Paving the way to hepatocellular carcinoma显示文摘Metabolic disorders are increasingly leading to non-alcoholic fatty liver disease,subsequent steatohepatitis,cirrhosis and hepatocellular carcinoma.Fibroblast growth factors and their receptors play an important role in maintaining metabolic homeostasis also in the liver and disorders in signaling have been identified to contribute to those pathophysiologic conditions leading to hepatic lipid accumulation and chronic inflammation.While specific and well tolerated inhibitors of fibroblast growth factor receptor activity are currently developed for(non-liver)cancer therapy,treatment of non-alcoholic fatty liver disease and nonalcoholic steatohepatitis is still limited.Fibroblast growth factor-mimicking or restoring approaches have recently evolved as a novel therapeutic option and the impact of such interactions with the fibroblast growth factor receptor signaling network during non-alcoholic fatty liver disease/non-alcoholic steatohepatitis development is reviewed here. | Matthias Ocker | 2020 | World Journal of Gastroenterology2020，26，3： | 5 |
| 5 | Hepatocellular carcinoma: Therapeutic advances in signaling,epigenetic and immune targets显示文摘Hepatocellular carcinoma(HCC)remains a global medical burden with rising incidence due to chronic viral hepatitis and non-alcoholic fatty liver diseases.Treatment of advanced disease stages is still unsatisfying.Besides first and second generation tyrosine kinase inhibitors,immune checkpoint inhibitors have become central for the treatment of HCC.New modalities like epigenetic therapy using histone deacetylase inhibitors(HDACi)and cell therapy approaches with chimeric antigen receptor T cells(CAR-T cells)are currently under investigation in clinical trials.Development of such novel drugs is closely linked to the availability and improvement of novel preclinical and animal models and the identification of predictive biomarkers.The current status of treatment options for advanced HCC,emerging novel therapeutic approaches and different preclinical models for HCC drug discovery and development are reviewed here. | Daniel Neureiter Sebastian Stintzing Tobias Kiesslich Matthias Ocker | 2019 | World Journal of Gastroenterology2019，25，25： | 4 |
| 6 | Biomarkers for hepatocellular carcinoma: What's new on the horizon?显示文摘Treatment of advanced hepatocellular carcinoma remains unsatisfying and so far only prognostic biomarkers like α-fetoprotein have been established. No clear predictive biomarker is currently available for standard of care therapies, including targeted therapies like sorafenib. Novel therapeutic options like immune checkpoint inhibitors may pose new challenges to identification and validation of such markers. Currently, PD-L1 expression via immunohistochemistry and tumor mutational burden via next-generation sequencing are explored as predictive biomarkers for these novel treatments. Limited tissue availability due to lack of biopsies still restricts the use of tissue based approaches. Novel methods exploring circulating or cell free nucleic acids(DNA, RNA or miRNAcontaining exosomes) could provide a new opportunity to establish predictive biomarkers. Epigenetic profiling and next-generation sequencing approaches from liquid biopsies are under development. Sample size, etiologic and geographical background need to be carefully addressed in such studies to achieve meaningful results that could be translated into clinical practice. Proteomics, metabolomics and molecular imaging are further emerging technologies. | Matthias Ocker | 2018 | World Journal of Gastroenterology2018，24，35： | 4 |
| 7 | Pancreatic cancer cells surviving gemcitabine treatment express markersof stem cell differentiation and epithelial-mesenchymal transition显示文摘 | Karl Quint Manuel Tonigold Pietro Di Fazio Roberta Montalbano Susanne Lingelbach Felix Rückert Beate Alinger Matthias Ocker Daniel Neureiter | 2012 | International Journal of Oncology2012，，6： | 2 |
| 8 | Combined in vitro antitumoral action of tamoxifen and retinoic acid derivatives in hepatoma cells显示文摘 | Herold C Ganslmayer M Ocker M | 2002 | Int J Oncol2002，20，1： | 1 |
| 9 | Combined in vitro antitumoral action of tamoxifen and retinoic acid derivatives in hepatoma cells显示文摘 | Herold C Ganslmayer M Ocker M | 2002 | IntJ Oncol2002，20，1： | 1 |
| 10 | The synthetic retinoid adapalene inhibits proliferation and induces apoptosis in colorectal cancer cells in vitro显示文摘 | OCKER M HEROLD C GANSLMAYER M | 2003 | Int J Cancer2003，107，3： | 1 |
| 11 | The research nurse role in a clinic-based oncology research setting显示文摘 | Ocker BM Plank DM | 2000 | Cancer Nurs2000，23，4： | 1 |
| 12 | Ciprofloxacin induces apoptosis and inhibits proliferation of human colorectal carcinoma cells显示文摘 | Herold C Ocker M Ganslmayer M | 2002 | Br J Cancer2002，86，3： | 1 |
| 13 | The synthetic retinoid adapalene inhibits proliferation and induces apoptosis in colorectal cancer cells in vitro显示文摘 | Ocker M Herold C Ganslmayer M | 2003 | Int J Cancer2003，107，： | 1 |
| 14 | bcl-2-specific siRNAs restore gemcitabine sensitivity in human pancreatic cancer cells显示文摘 | Okamoto K Ocker M Neureiter D | | 0，，03： | 1 |
| 15 | Histone deacetylase inhibitors: signalling towards p21^cip1/waf1显示文摘 | Ocker M Schneider S R | 2007 | Int J Biochem Cell Biol2007，39，78： | 1 |
| 16 | Combined in vitro anti-tumoral action of tamoxifen and retinoic acid derivatives in hepatoma cells显示文摘 | Herold C Ganslmayer M Ocker M | 2002 | Int J Oncol2002，20，1： | 1 |
| 17 | The pan?deacetylase inhibitor panobinostat modulates the expressionof epithelial?mesenchymal transition markers in hepatocellular carcinoma models显示文摘 | Pietro Di Fazio Roberta Montalbano Karl Quint Beate Alinger Ralf Kemmerling Tobias Kiesslich Matthias Ocker Daniel Neureiter | 2013 | Oncology Letters2013，，1： | 1 |
| 18 | CD22 is a negative regula- tor of B-cell receptor signalling 显示文摘 | Nitschke L Carsetti R Ocker B | 1997 | Curr Biol1997，7，2： | 1 |
| 19 | Differentiation patterning of vascular smooth muscle cells(VSMC) in ather- osclerosis显示文摘 | Stintzing S Ocker M Hartner A | 2009 | Virchows Arch2009，455，2： | 1 |
| 20 | Passage efficiency of adult Pacific lampreys at hydropower dams on the lower Columbia River显示文摘 | MOSER M L OCKER P A STEUHRENBERG L C | 2002 | Transactions of the A- merican Fisheries Society2002，131，5： | 1 |
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