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  1. Artikel ; Online: Reply.

    Boike, Justin R / Thornburg, Bartley / Vanwagner, Lisa B

    Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association

    2022  Band 21, Heft 6, Seite(n) 1674–1675

    Sprache Englisch
    Erscheinungsdatum 2022-09-13
    Erscheinungsland United States
    Dokumenttyp Letter ; Comment
    ZDB-ID 2119789-1
    ISSN 1542-7714 ; 1542-3565
    ISSN (online) 1542-7714
    ISSN 1542-3565
    DOI 10.1016/j.cgh.2022.09.003
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Patients transplanted for nonalcoholic steatohepatitis are at increased risk for postoperative cardiovascular events.

    Vanwagner, Lisa B / Bhave, Manali / Te, Helen S / Feinglass, Joe / Alvarez, Lisa / Rinella, Mary E

    Hepatology (Baltimore, Md.)

    2012  Band 56, Heft 5, Seite(n) 1741–1750

    Abstract: Unlabelled: Nonalcoholic steatohepatitis (NASH) is an independent predictor of coronary artery disease (CAD). Our aim was to compare the incidence of cardiovascular (CV) events between patients transplanted for NASH and alcohol (ETOH)-induced cirrhosis. ...

    Abstract Unlabelled: Nonalcoholic steatohepatitis (NASH) is an independent predictor of coronary artery disease (CAD). Our aim was to compare the incidence of cardiovascular (CV) events between patients transplanted for NASH and alcohol (ETOH)-induced cirrhosis. This is a retrospective cohort study (August 1993 to March 2010) of 242 patients (115 NASH and 127 ETOH) with ≥12 months follow-up after liver transplantation (LT). Those with hepatocellular carcinoma or coexisting liver diseases were excluded. Kaplan-Meier's and Cox's proportional hazard analyses were conducted to compare survival. Logistic regression was used to calculate the likelihood of CV events, defined as death from any cardiac cause, myocardial infarction, acute heart failure, cardiac arrest, arrhythmia, complete heart block, and/or stroke requiring hospitalization <1 year after LT. Patients in the NASH group were older (58.4 versus 53.3 years) and were more likely to be female (45% versus 18%; P < 0.001). They were more likely to be morbidly obese (32% versus 9%), have dyslipidemia (25% versus 6%), or have hypertension (53% versus 38%; P < 0.01). On multivariate analysis, NASH patients were more likely to have a CV event <1 year after LT, compared to ETOH patients, even after controlling for recipient age, sex, smoking status, pretransplant diabetes, CV disease, and the presence of metabolic syndrome (26% versus 8%; odds ratio = 4.12; 95% confidence interval = 1.91-8.90). The majority (70%) of events occurred in the perioperative period, and the occurrence of a CV event was associated with a 50% overall mortality. However, there were no differences in patient, graft, or CV mortality between groups.
    Conclusions: CV complications are common after LT, and NASH patients are at increased risk independent of traditional cardiac risk factors, though this did not affect overall mortality.
    Mesh-Begriff(e) Aged ; Arrhythmias, Cardiac/epidemiology ; Cardiovascular Diseases/epidemiology ; Cardiovascular Diseases/mortality ; Dyslipidemias/complications ; Dyslipidemias/epidemiology ; Fatty Liver/complications ; Fatty Liver/mortality ; Fatty Liver/surgery ; Female ; Heart Arrest/epidemiology ; Heart Block/epidemiology ; Heart Failure/epidemiology ; Hospitalization ; Humans ; Hypertension/complications ; Hypertension/epidemiology ; Incidence ; Kaplan-Meier Estimate ; Liver Cirrhosis, Alcoholic/complications ; Liver Cirrhosis, Alcoholic/mortality ; Liver Cirrhosis, Alcoholic/surgery ; Liver Transplantation/adverse effects ; Logistic Models ; Male ; Middle Aged ; Myocardial Infarction/epidemiology ; Non-alcoholic Fatty Liver Disease ; Obesity, Morbid/complications ; Obesity, Morbid/epidemiology ; Proportional Hazards Models ; Retrospective Studies ; Risk Factors ; Stroke/epidemiology
    Sprache Englisch
    Erscheinungsdatum 2012-11
    Erscheinungsland United States
    Dokumenttyp Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 604603-4
    ISSN 1527-3350 ; 0270-9139
    ISSN (online) 1527-3350
    ISSN 0270-9139
    DOI 10.1002/hep.25855
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: Activation of the insulin-like growth factor-1 receptor induces resistance to epidermal growth factor receptor antagonism in head and neck squamous carcinoma cells.

    Jameson, Mark J / Beckler, Andrew D / Taniguchi, Linnea E / Allak, Amir / Vanwagner, Lisa B / Lee, Nora G / Thomsen, William C / Hubbard, Matthew A / Thomas, Christopher Y

    Molecular cancer therapeutics

    2011  Band 10, Heft 11, Seite(n) 2124–2134

    Abstract: Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKI) have poor efficacy in head and neck squamous carcinoma cells (HNSCC). Because the IGF-1 receptor (IGF1R) generates potent prosurvival signals and has been implicated in therapeutic ... ...

    Abstract Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKI) have poor efficacy in head and neck squamous carcinoma cells (HNSCC). Because the IGF-1 receptor (IGF1R) generates potent prosurvival signals and has been implicated in therapeutic resistance, its ability to induce resistance to EGFR-TKIs was studied in vitro. Five HNSCC cell lines showed reduced sensitivity to the EGFR-TKI gefitinib when the IGF1R was activated. In SCC-25 and Cal27 cells, gefitinib inhibited basal and EGF-stimulated EGFR, extracellular signal-regulated kinase (Erk), and Akt phosphorylation and reduced cell number. This correlated with initiation of apoptosis based on a 4-fold increase in PARP cleavage and a 2.5-fold increase in Annexin V positivity. The apoptotic response and reduction in cell number were blocked by IGF1R activation, which resulted in phosphorylation of both Erk and Akt. In both the cell lines, IGF1R-induced Erk, but not Akt, activation was eliminated by gefitinib. IGF1R-induced gefitinib resistance was unaffected by MAP/Erk kinase inhibition with U0126 but was partially impaired by inhibition of phosphoinositide-3-kinase with LY294002. The IGF1R-TKI PQ401 inhibited growth of SCC-25 and Cal27 cells alone and also acted synergistically with gefitinib. Thus, the IGF1R can make HNSCC cells resistant to EGFR-TKI treatment via a prosurvival mechanism. Of the 8 HNSCC tumor samples studied, all samples expressed the IGF1R and 5 showed detectable IGF1R phosphorylation, suggesting that this receptor may be relevant in vivo, and thus, combined EGFR/IGF1R inhibition may be necessary in some patients for effective targeted molecular therapy.
    Mesh-Begriff(e) Animals ; Antineoplastic Agents/pharmacology ; Apoptosis/drug effects ; Carcinoma, Squamous Cell/genetics ; Carcinoma, Squamous Cell/metabolism ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cell Survival/drug effects ; Drug Resistance, Neoplasm/genetics ; Enzyme Activation ; ErbB Receptors/antagonists & inhibitors ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Head and Neck Neoplasms/genetics ; Head and Neck Neoplasms/metabolism ; Humans ; Protein Kinase Inhibitors/pharmacology ; Proto-Oncogene Proteins c-akt/metabolism ; Rats ; Receptor, IGF Type 1/antagonists & inhibitors ; Receptor, IGF Type 1/genetics ; Receptor, IGF Type 1/metabolism ; Signal Transduction/drug effects ; Squamous Cell Carcinoma of Head and Neck
    Chemische Substanzen Antineoplastic Agents ; Protein Kinase Inhibitors ; ErbB Receptors (EC 2.7.10.1) ; Receptor, IGF Type 1 (EC 2.7.10.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24)
    Sprache Englisch
    Erscheinungsdatum 2011-08-30
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2063563-1
    ISSN 1538-8514 ; 1535-7163
    ISSN (online) 1538-8514
    ISSN 1535-7163
    DOI 10.1158/1535-7163.MCT-11-0294
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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