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  • 1
    UID:
    (DE-627)1811125344
    Format: 7
    ISSN: 1096-0945
    Content: The present review is based on the research presented at the symposium dedicated to the legacy of the two scientists that made important discoveries in the field of alcohol-induced liver damage: Professors C.S. Lieber and S.W. French. The invited speakers described pharmacological, toxicological and patho-physiological effects of alcohol misuse. Moreover, genetic biomarkers determining adverse drug reactions due to interactions between therapeutics used for chronic or infectious diseases and alcohol exposure were discussed. The researchers presented their work in areas of alcohol-induced impairment in lipid protein trafficking and endocytosis, as well as the role of lipids in the development of fatty liver. The researchers showed that alcohol leads to covalent modifications that promote hepatic dysfunction and injury. We concluded that using new advanced techniques and research ideas leads to important discoveries in science.
    Note: Gesehen am 21.07.2022
    In: Experimental and molecular pathology, Orlando, Fla. : Academic Press, 1962, 126(2022) vom: Juni, Artikel-ID 104750, Seite 1-7, 1096-0945
    In: volume:126
    In: year:2022
    In: month:06
    In: elocationid:104750
    In: pages:1-7
    In: extent:7
    Language: English
    URL: Volltext  (lizenzpflichtig)
    URL: Volltext  (lizenzpflichtig)
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  • 2
    UID:
    (DE-627)1572479027
    Format: 19
    ISSN: 1096-0945
    Content: This paper is based upon the “8th Charles Lieber's Satellite Symposium” organized by Manuela G. Neuman at the Research Society on Alcoholism Annual Meeting, on June 25, 2016 at New Orleans, Louisiana, USA. The integrative symposium investigated different aspects of alcohol-induced liver disease (ALD) as well as non-alcohol-induced liver disease (NAFLD) and possible repair. We revealed the basic aspects of alcohol metabolism that may be responsible for the development of liver disease as well as the factors that determine the amount, frequency and which type of alcohol misuse leads to liver and gastrointestinal diseases.
    Note: Gesehen am 30.04.2018
    In: Experimental and molecular pathology, Orlando, Fla. : Academic Press, 1962, 102(2017), 1, Seite 162-180, 1096-0945
    In: volume:102
    In: year:2017
    In: number:1
    In: pages:162-180
    In: extent:19
    Language: English
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  • 3
    UID:
    (DE-627)1736877585
    Format: 19
    ISSN: 1096-0945
    Content: This paper is based upon the “Charles Lieber Satellite Symposia” organized by Manuela G. Neuman at the Research Society on Alcoholism (RSA) Annual Meetings, 2013 and 2014. The present review includes pre-clinical, translational and clinical research that characterize alcoholic liver disease (ALD) and non-alcoholic steatohepatitis (NASH). In addition, a literature search in the discussed area was performed. Strong clinical and experimental evidence lead to recognition of the key toxic role of alcohol in the pathogenesis of ALD. The liver biopsy can confirm the etiology of NASH or alcoholic steatohepatitis (ASH) and assess structural alterations of cells, their organelles, as well as inflammatory activity. Three histological stages of ALD are simple steatosis, ASH, and chronic hepatitis with hepatic fibrosis or cirrhosis. These latter stages may also be associated with a number of cellular and histological changes, including the presence of Mallory's hyaline, megamitochondria, or perivenular and perisinusoidal fibrosis. Genetic polymorphisms of ethanol metabolizing enzymes such as cytochrome p450 (CYP) 2E1 activation may change the severity of ASH and NASH. Alcohol mediated hepatocarcinogenesis, immune response to alcohol in ASH, as well as the role of other risk factors such as its co-morbidities with chronic viral hepatitis in the presence or absence of human immunodeficiency virus are discussed. Dysregulation of hepatic methylation, as result of ethanol exposure, in hepatocytes transfected with hepatitis C virus (HCV), illustrates an impaired interferon signaling. The hepatotoxic effects of ethanol undermine the contribution of malnutrition to the liver injury. Dietary interventions such as micro and macronutrients, as well as changes to the microbiota are suggested. The clinical aspects of NASH, as part of metabolic syndrome in the aging population, are offered. The integrative symposia investigate different aspects of alcohol-induced liver damage and possible repair. We aim to (1) determine the immuno-pathology of alcohol-induced liver damage, (2) examine the role of genetics in the development of ASH, (3) propose diagnostic markers of ASH and NASH, (4) examine age differences, (5) develop common research tools to study alcohol-induced effects in clinical and pre-clinical studies, and (6) focus on factors that aggravate severity of organ-damage. The intention of these symposia is to advance the international profile of the biological research on alcoholism. We also wish to further our mission of leading the forum to progress the science and practice of translational research in alcoholism.
    Note: Gesehen am 28.10.2020
    In: Experimental and molecular pathology, Orlando, Fla. : Academic Press, 1962, 97(2014), 3, Seite 492-510, 1096-0945
    In: volume:97
    In: year:2014
    In: number:3
    In: pages:492-510
    In: extent:19
    Language: English
    URL: Volltext  (lizenzpflichtig)
    URL: Volltext  (lizenzpflichtig)
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  • 4
    UID:
    (DE-627)1727170431
    Format: 15
    ISSN: 1096-0945
    Content: The present review spans a broad spectrum of topics dealing with alcoholic liver disease (ALD), including clinical research, translational research, pathogenesis and therapies. A special accent is placed on alcohol misuse, as alcohol is a legally commercialized and taxable product. Drinking alcohol, particularly from a young age, is a major health problem. Alcoholism is known to contribute to morbidity and mortality. A systematic literature search was performed in order to obtain updated data (2008-2015). The review is focused on genetic polymorphisms of alcohol metabolizing enzymes and the role of cytochrome p450 2E1 and iron in ALD. Alcohol-mediated hepatocarcinogenesis is also discussed in the presence or absence of co-morbidities such as viral hepatitis C as well as therapeutic the role of innate immunity in ALD-HCV. Moreover, emphasis was placed on alcohol and drug interactions, as well as liver transplantation for end-stage ALD. Finally, the time came to eradicate alcohol-induced liver and intestinal damage by using betaine.
    Note: Gesehen am 17.08.2020
    In: Experimental and molecular pathology, Orlando, Fla. : Academic Press, 1962, 99(2015), 3, Seite 596-610, 1096-0945
    In: volume:99
    In: year:2015
    In: number:3
    In: pages:596-610
    In: extent:15
    Language: English
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  • 5
    UID:
    (DE-627)1693727781
    ISSN: 1096-0945
    Content: Colorectal cancer (CRC) is the third most common carcinoma worldwide. Despite the progress in screening and treatment, CRC remains a leading cause of cancer-related mortality. Alterations to normal nucleic acid processing may drive neoplastic transformation of colorectal epithelium. DNA repair machinery performs an essential function in the protection of genome by reducing the number of genetic polymorphisms/variations that may drive carcinogenicity. Four essential DNA repair systems are known which include nucleotide excision repair (NER), base excision repair (BER), mismatch repair (MMR), and double-strand break repair (DSBR). Polymorphisms of DNA repair genes have been shown to influence the risk of cancer development as well as outcomes of treatment. Several studies demonstrated the association between genetic polymorphism of DNA repair genes and increased risk of CRC in different populations. In this review, we have summarized the impact of DNA repair gene polymorphisms on risk of CRC development and treatment outcomes. Advancements of the current understanding for the impact of DNA repair gene polymorphisms on the risk and treatment of CRC may support diagnostic and predictive roles in patients with CRC.
    Note: Available online 24 December 2019 , Gesehen am 01.04.2020
    In: Experimental and molecular pathology, Orlando, Fla. : Academic Press, 1962, 113(2019) Artikel-Nummer 104364, 13 Seiten, 1096-0945
    In: volume:113
    In: year:2020
    Language: English
    URL: Volltext  (lizenzpflichtig)
    URL: Volltext  (lizenzpflichtig)
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  • 6
    UID:
    (DE-627)1795143517
    Format: 6
    ISSN: 1096-0945
    Content: Lynch syndrome (LS) is caused by a pathogenic heterozygous germline variant in one of the DNA mismatch repair (MMR) genes: MLH1, MSH2, MSH6 or PMS2. LS-associated colorectal carcinomas (CRCs) are characterized by MMR deficiency and by accumulation of multiple insertions/deletions at coding microsatellites (cMS). MMR deficiency-induced variants at defined cMS loci have a driver function and promote tumorigenesis. Notably, PMS2 variant carriers face only a slightly increased risk of developing CRC. Here, we investigate whether this lower penetrance is also reflected by differences in molecular features and cMS variant patterns. Tumor DNA was extracted from formalin-fixed paraffin-embedded (FFPE) tissue cores or sections (n = 90). Tumors originated from genetically proven germline pathogenic MMR variant carriers (including 14 PMS2-deficient tumors). The mutational spectrum was analyzed using fluorescently labeled primers specific for 18 cMS previously described as mutational targets in MMR-deficient tumors. Immune cell infiltration was analyzed by immunohistochemical detection of T-cells on FFPE tissue sections. The cMS spectrum of PMS2-deficient CRCs did not show any significant differences from MLH1/MSH2-deficient CRCs. PMS2-deficient tumors, however, displayed lower CD3-positive T-cell infiltration compared to other MMR-deficient cancers (28.00 vs. 55.00 per 0.1 mm2, p = 0.0025). Our study demonstrates that the spectrum of potentially immunogenic cMS variants in CRCs from PMS2 gene variant carriers is similar to that observed in CRCs from other MMR gene variant carriers. Lower immune cell infiltration observed in PMS2-deficient CRCs could be the result of alternative mechanisms of immune evasion or immune cell exclusion, similar to those seen in MMR-proficient tumors.
    Note: Available online 22 July 2021 , Gesehen am 09.03.2022
    In: Experimental and molecular pathology, Orlando, Fla. : Academic Press, 1962, 122(2021), Artikel-ID 104668, Seite 1-6, 1096-0945
    In: volume:122
    In: year:2021
    In: elocationid:104668
    In: pages:1-6
    In: extent:6
    Language: English
    URL: Volltext  (lizenzpflichtig)
    URL: Volltext  (lizenzpflichtig)
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  • 7
    UID:
    (DE-627)1582466645
    Format: 7
    ISSN: 1096-0945
    Content: Primary meningeal melanocytic tumors have genetic similarities with uveal melanomas, including GNAQ or GNA11 mutations. While BAP1 mutations and loss of chromosome 3 have adverse prognostic meaning in uveal melanoma, genetic alterations associated with metastasis have not been investigated in primary meningeal melanocytic tumors. We describe a 43-year-old female with a GNAQ-mutated, BAP1-wt melanocytic tumor originating in the parietal brain region and liver metastases 4years after initial diagnosis. After repeated surgery and chemotherapy she was treated with the immunomodulatory agent ipilimumab. Tissue from the primary and recurrent intracranial tumor (histologically originally diagnosed as intermediate-grade melanocytoma resp. melanoma) and from the liver metastasis was investigated for genome-wide copy number variations and DNA methylation profile. Complete loss of 10p and 19p, partial loss of 16p and a small deletion on 10q were only present in the liver metastasis and not in the intracranial tumors. The DNA methylation profiles of the intracranial tumors and the liver metastasis resembled those of meningeal melanocytomas. In conclusion, in this report we show that a distant metastasis of a meningeal melanocytic tumor has a similar methylation profile as the primary tumor and suggest that particular copy number variations may be associated with metastatic behavior.
    Note: Available online 11 December 2016 , Gesehen am 31.10.2018
    In: Experimental and molecular pathology, Orlando, Fla. : Academic Press, 1962, 102(2017), 1, Seite 25-31, 1096-0945
    In: volume:102
    In: year:2017
    In: number:1
    In: pages:25-31
    In: extent:7
    Language: English
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  • 8
    Online Resource
    Online Resource
    Orlando, Fla. : Academic Press | Amsterdam [u.a.] : Elsevier ; 1.1962 -
    UID:
    (DE-627)266016693
    Format: Online-Ressource
    ISSN: 1096-0945
    Note: Gesehen am 23.08.2023
    Additional Edition: 0014-4800
    Additional Edition: Erscheint auch als Druck-Ausgabe Experimental and molecular pathology Amsterdam [u.a.] : Elsevier, 1962 0014-4800
    Language: English
    Keywords: Pathobiochemie ; Zeitschrift ; Online-Ressource ; Molekularpathologie ; Zeitschrift ; Online-Ressource ; Pathobiochemie ; Zeitschrift ; Molekularpathologie ; Zeitschrift ; Pathologie ; Zeitschrift ; Zeitschrift
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  • 9
    Journal/Serial
    Journal/Serial
    Amsterdam [u.a.] : Elsevier | New York, NY [u.a.] | San Diego, Calif. [u.a.] : Academic Press ; 1.1962 -
    UID:
    (DE-602)gbv_129497916
    ISSN: 0014-4800
    Additional Edition: ISSN 1096-0945
    Additional Edition: Erscheint auch als Online-Ausg. Experimental and molecular pathology Orlando, Fla. : Academic Press, 1962 ISSN 1096-0945
    Language: English
    Keywords: Pathobiochemie ; Zeitschrift ; Molekularpathologie ; Zeitschrift ; Pathologie ; Zeitschrift ; Zeitschrift
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  • 10
    Journal/Serial
    Journal/Serial
    Amsterdam [u.a.] : Elsevier | New York, NY [u.a.] | San Diego, Calif. [u.a.] : Academic Press ; 1.1962 -
    UID:
    (DE-627)129497916
    ISSN: 0014-4800
    Additional Edition: 1096-0945
    Additional Edition: Erscheint auch als Online-Ausg. Experimental and molecular pathology Orlando, Fla. : Academic Press, 1962 1096-0945
    Language: English
    Keywords: Pathobiochemie ; Zeitschrift ; Molekularpathologie ; Zeitschrift ; Pathologie ; Zeitschrift ; Zeitschrift
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