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  1. Book ; Thesis: Bile acid attenuate progression of pancreatic precursor lesions via Farnesoid X receptor in a mouse model

    Xu, Zhen / Fortunato, Franco

    2021  

    Institution Universität Heidelberg
    Author's details vorgelegt von Zhen Xu ; Doktorvater: Herr PD. Dr. Franco Fortunato
    Language English
    Size vi, 73 Blätter, Illustrationen, Diagramme
    Publishing place Heidelberg
    Publishing country Germany
    Document type Book ; Thesis
    Thesis / German Habilitation thesis Dissertation, Ruprecht-Karls-Universität Heidelberg, 2021
    HBZ-ID HT021121645
    Database Catalogue ZB MED Medicine, Health

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  2. Book ; Thesis: Chronic lipopolysaccharide exposure accelerates Kras G12D induced pancreatic tumorigenesis via upregulation of tumor-promoting factors

    Huang, Zhenhua / Fortunato, Franco

    2022  

    Institution Universität Heidelberg
    Author's details vorgelegt von Zhenhua Huang ; Doktorvater: Herr PD Dr. Franco Fortunato
    Subject code 616.994 ; 610 ; 570
    Language English
    Size viii, 109 Seiten, Illustrationen, Diagramme
    Publishing place Heidelberg
    Publishing country Germany
    Document type Book ; Thesis
    Thesis / German Habilitation thesis Dissertation, Ruprecht-Karls-Universität Heidelberg, 2023
    HBZ-ID HT030722430
    Database Catalogue ZB MED Medicine, Health

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  3. Book ; Online ; Thesis: Tumor biomarkers that identify molecular subtypes and best responders to chemotherapy in patients with PDAC

    Zhou, Xu [Verfasser] / Fortunato, Franco [Akademischer Betreuer]

    2023  

    Author's details Xu Zhou ; Betreuer: Franco Fortunato
    Keywords Medizin, Gesundheit ; Medicine, Health
    Subject code sg610
    Language English
    Publisher Universitätsbibliothek Heidelberg
    Publishing place Heidelberg
    Document type Book ; Online ; Thesis
    Database Digital theses on the web

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  4. Article ; Online: H

    Chen, Cheng / Wang, Shijin / Yu, Linna / Mueller, Johannes / Fortunato, Franco / Rausch, Vanessa / Mueller, Sebastian

    Redox biology

    2021  Volume 46, Page(s) 102081

    Abstract: Background: Alcoholic liver disease (ALD) is the most common liver disease worldwide and its underlying molecular mechanisms are still poorly understood. Moreover, conflicting data have been reported on potentially protective autophagy, the exact role ... ...

    Abstract Background: Alcoholic liver disease (ALD) is the most common liver disease worldwide and its underlying molecular mechanisms are still poorly understood. Moreover, conflicting data have been reported on potentially protective autophagy, the exact role of ethanol-metabolizing enzymes and ROS.
    Methods: Expression of LC3B, CYP2E1, and NOX4 was studied in a mouse model of acute ethanol exposure by immunoblotting and immunohistochemistry. Autophagy was further studied in primary mouse hepatocytes and huh7 cells in response to ethanol and its major intermediator acetaldehyde. Experiments were carried out in cells overexpressing CYP2E1 and knock down of NOX4 using siRNA. The response to external H
    Results: Acute ethanol exposure of mice over 24 h significantly induced autophagy as measured by LC3B expression but also induced the ROS-generating CYP2E1 and NOX4 enzymes. Notably, ethanol but not its downstream metabolite acetaldehyde induced autophagy in primary mouse hepatocytes. In contrast, autophagy could only be induced in huh7 cells in the presence of overexpressed CYP2E1. In addition, overexpression of NOX4 also significantly increased autophagy, which could be blocked by siRNA mediated knock down. The antioxidant N-acetylcysteine (NAC) also efficiently blocked CYP2E1-and NOX4-mediated induction of autophagy. Finally, specific and non-toxic production of H
    Conclusion: We here provide evidence that short-term ethanol exposure induces autophagy in hepatocytes both in vivo and in vitro through the generation of ROS. These data suggest that suppression of autophagy by ethanol is most likely due to longer alcohol exposure during chronic alcohol consumption with the accumulation of e.g. misfolded proteins.
    MeSH term(s) Animals ; Autophagy ; Cytochrome P-450 CYP2E1/genetics ; Ethanol/toxicity ; Hydrogen Peroxide ; Liver Diseases, Alcoholic/genetics ; Mice
    Chemical Substances Ethanol (3K9958V90M) ; Hydrogen Peroxide (BBX060AN9V) ; Cytochrome P-450 CYP2E1 (EC 1.14.13.-)
    Language English
    Publishing date 2021-07-24
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2701011-9
    ISSN 2213-2317 ; 2213-2317
    ISSN (online) 2213-2317
    ISSN 2213-2317
    DOI 10.1016/j.redox.2021.102081
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Farnesoid X receptor activation inhibits pancreatic carcinogenesis.

    Xu, Zhen / Huang, Zhenhua / Zhang, Yifan / Sun, Haitao / Hinz, Ulf / Heger, Ulrike / Loos, Martin / Gonzalez, Frank J / Hackert, Thilo / Bergmann, Frank / Fortunato, Franco

    Biochimica et biophysica acta. Molecular basis of disease

    2023  Volume 1869, Issue 7, Page(s) 166811

    Abstract: Farnesoid X receptor (FXR), a member of the nuclear receptor superfamily that controls bile acid (BA) homeostasis, has also been proposed as a tumor suppressor for breast and liver cancer. However, its role in pancreatic ductal adenocarcinoma (PDAC) ... ...

    Abstract Farnesoid X receptor (FXR), a member of the nuclear receptor superfamily that controls bile acid (BA) homeostasis, has also been proposed as a tumor suppressor for breast and liver cancer. However, its role in pancreatic ductal adenocarcinoma (PDAC) tumorigenesis remains controversial. We recently found that FXR attenuates acinar cell autophagy in chronic pancreatitis resulting in reduced autophagy and promotion of pancreatic carcinogenesis. Feeding Kras-p48-Cre (KC) mice with the BA chenodeoxycholic acid (CDCA), an FXR agonist, attenuated pancreatic intraepithelial neoplasia (PanIN) progression, reduced cell proliferation, neoplastic cells and autophagic activity, and increased acinar cells, elevated pro-inflammatory cytokines and chemokines, with a compensatory increase in the anti-inflammatory response. Surprisingly, FXR-deficient KC mice did not show any response to CDCA, suggesting that CDCA attenuates PanIN progression and decelerate tumorigenesis in KC mice through activating pancreatic FXR. FXR is activated in pancreatic cancer cell lines in response to CDCA in vitro. FXR levels were highly increased in adjuvant and neoadjuvant PDAC tissue compared to healthy pancreatic tissue, indicating that FXR is expressed and potentially activated in human PDAC. These results suggest that BA exposure activates inflammation and suppresses autophagy in KC mice, resulting in reduced PanIN lesion progression. These data suggest that activation of pancreatic FXR has a protective role by reducing the growth of pre-cancerous PDAC lesions in response to CDCA and possibly other FXR agonists.
    MeSH term(s) Humans ; Mice ; Animals ; Pancreas/pathology ; Pancreatic Neoplasms/pathology ; Carcinogenesis/genetics ; Carcinogenesis/pathology ; Carcinoma, Pancreatic Ductal/genetics ; Cell Transformation, Neoplastic/pathology ; Chenodeoxycholic Acid/pharmacology ; Bile Acids and Salts
    Chemical Substances Chenodeoxycholic Acid (0GEI24LG0J) ; Bile Acids and Salts
    Language English
    Publishing date 2023-07-27
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Intramural
    ZDB-ID 60-7
    ISSN 1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    ISSN (online) 1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
    ISSN 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    DOI 10.1016/j.bbadis.2023.166811
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: Retrospective electron microscopy: Preservation of fine structure by freezing and aldehyde fixation.

    Fortunato, Franco / Hackert, Thilo / Büchler, Markus W / Kroemer, Guido

    Molecular & cellular oncology

    2016  Volume 3, Issue 6, Page(s) e1251382

    Abstract: For many years it has been believed that ultrastructural analysis by transmission electron microscopy (TEM) is not possible using frozen tissues. We have developed a TEM method that allows the evaluation of organelles using pancreatic tissue that was ... ...

    Abstract For many years it has been believed that ultrastructural analysis by transmission electron microscopy (TEM) is not possible using frozen tissues. We have developed a TEM method that allows the evaluation of organelles using pancreatic tissue that was previously liquid nitrogen snap-frozen and stored long-term at -80°C. This method is suitable for the quantitative assessment of mitochondria, rough endoplasmic reticulum (RER), and Golgi structures, as well as organelles originating from autophagy signaling. Frozen pancreatic tissue exhibited no signs of freezing- or storage-related damage and was undistinguishable from fresh material subjected to standard glutaraldehyde fixation. Since pancreatic tissue is the most delicate tissue to work with due to the high expression of digestive enzymes, our method is also suitable for other tissue types such as liver. Thus, by applying proper tissue freezing and fixation techniques, retrospective TEM analysis can be performed on mammalian tissues in a time- and cost-saving manner.
    Language English
    Publishing date 2016-10-27
    Publishing country United States
    Document type Journal Article
    ISSN 2372-3556
    ISSN 2372-3556
    DOI 10.1080/23723556.2016.1251382
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Tumor and stroma COL8A1 secretion induces autocrine and paracrine progression signaling in pancreatic ductal adenocarcinoma.

    Yan, Bin / Liu, Li / Zhao, Lian / Hinz, Ulf / Luo, Yiqiao / An, Xuefeng / Gladkich, Jury / de la Torre, Carolina / Huang, Zhenhua / Schrapel, Daniel / Gross, Wolfgang / Fortunato, Franco / Schaefer, Michael / Gaida, Matthias M / Herr, Ingrid

    Matrix biology : journal of the International Society for Matrix Biology

    2022  Volume 114, Page(s) 84–107

    Abstract: Several collagen subtypes are involved in pancreatic ductal adenocarcinoma (PDAC) desmoplasia, which constrains therapeutic efficacy. We evaluated collagen type VIII alpha 1 chain (COL8A1), whose function in PDAC is currently unknown. We identified ... ...

    Abstract Several collagen subtypes are involved in pancreatic ductal adenocarcinoma (PDAC) desmoplasia, which constrains therapeutic efficacy. We evaluated collagen type VIII alpha 1 chain (COL8A1), whose function in PDAC is currently unknown. We identified COL8A1 expression in 7 examined PDAC cell lines by microarray analysis, western blotting, and RT‒qPCR. Higher COL8A1 expression occurred in 2 gemcitabine-resistant PDAC cell lines; pancreas tissue (n=15) from LSL-Kras
    MeSH term(s) Animals ; Humans ; Mice ; Adenocarcinoma/genetics ; Adenocarcinoma/metabolism ; Carcinoma, Pancreatic Ductal/genetics ; Carcinoma, Pancreatic Ductal/metabolism ; Cell Line, Tumor ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/metabolism ; Phosphatidylinositol 3-Kinases ; RNA, Small Interfering ; Collagen Type VIII/metabolism ; Pancreatic Neoplasms
    Chemical Substances Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; RNA, Small Interfering ; Col8A1 protein, human ; Collagen Type VIII
    Language English
    Publishing date 2022-11-11
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1183793-7
    ISSN 1569-1802 ; 0945-053X
    ISSN (online) 1569-1802
    ISSN 0945-053X
    DOI 10.1016/j.matbio.2022.11.002
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  8. Article ; Online: Impaired autophagosome-lysosome fusion in the pathogenesis of pancreatitis.

    Fortunato, Franco / Kroemer, Guido

    Autophagy

    2009  Volume 5, Issue 6, Page(s) 850–853

    Abstract: In contrast to apoptosis, necrosis is generally viewed as a pro-inflammatory cell death mechanism. Accumulation of autophagosomes and massive acinar cell necrosis is observed in human acute pancreatitis, a severe and potentially lethal inflammatory ... ...

    Abstract In contrast to apoptosis, necrosis is generally viewed as a pro-inflammatory cell death mechanism. Accumulation of autophagosomes and massive acinar cell necrosis is observed in human acute pancreatitis, a severe and potentially lethal inflammatory condition. We have investigated the incidence of apoptosis, autophagy and necrosis affecting acinar cells in a rat model of acute pancreatitis induced by chronic alcohol intake and acute endotoxemia. We have observed that the combination of alcohol exposure and endotoxemia results in substantial accumulation of autophagosomes without an increase in autolysosomes, coupled to the depletion of LAMP-2, a lysosomal protein required for the proper fusion of autophagosomes with lysosomes. Alcohol plus endotoxemia favors the switch from apoptotic to necrotic cell death, as indicated by histopathological examination, reduced ATP levels, suppressed caspase activation, as well as the nuclear release of the proinflammatory factor HMGB1. Importantly, patients with alcoholic pancreatitis also exhibit local LAMP-2 depletion, recapitulating the results obtained in the animal model. We suggest that acinar cell vacuolization in pancreatitis is mediated by an endotoxemia-induced depletion of LAMP-2, which in turn facilitates the accumulation of autophagosomes due to the deficient formation of autolysosomes. Hence, we postulate that the depletion of lysosomal proteins may play a critical role in the pathogenesis of acute pancreatitis.
    MeSH term(s) Animals ; Humans ; Lysosomal-Associated Membrane Protein 2/metabolism ; Lysosomes/metabolism ; Lysosomes/pathology ; Membrane Fusion ; Models, Biological ; Necrosis ; Pancreatitis/pathology ; Phagosomes/metabolism ; Phagosomes/pathology ; Phagosomes/ultrastructure ; Rats
    Chemical Substances Lysosomal-Associated Membrane Protein 2
    Language English
    Publishing date 2009-08-23
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2454135-7
    ISSN 1554-8635 ; 1554-8627
    ISSN (online) 1554-8635
    ISSN 1554-8627
    DOI 10.4161/auto.8839
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    Zs.A 6741: Show issues Location:
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  9. Article ; Online: Persister cell phenotypes contribute to poor patient outcomes after neoadjuvant chemotherapy in PDAC.

    Zhou, Xu / An, Jingyu / Kurilov, Roma / Brors, Benedikt / Hu, Kai / Peccerella, Teresa / Roessler, Stephanie / Pfütze, Katrin / Schulz, Angela / Wolf, Stephan / Hohmann, Nicolas / Theile, Dirk / Sauter, Max / Burhenne, Jürgen / Ei, Shigenori / Heger, Ulrike / Strobel, Oliver / Barry, Simon T / Springfeld, Christoph /
    Tjaden, Christine / Bergmann, Frank / Büchler, Markus / Hackert, Thilo / Fortunato, Franco / Neoptolemos, John P / Bailey, Peter

    Nature cancer

    2023  Volume 4, Issue 9, Page(s) 1362–1381

    Abstract: Neoadjuvant chemotherapy can improve the survival of individuals with borderline and unresectable pancreatic ductal adenocarcinoma; however, heterogeneous responses to chemotherapy remain a significant clinical challenge. Here, we performed RNA ... ...

    Abstract Neoadjuvant chemotherapy can improve the survival of individuals with borderline and unresectable pancreatic ductal adenocarcinoma; however, heterogeneous responses to chemotherapy remain a significant clinical challenge. Here, we performed RNA sequencing (n = 97) and multiplexed immunofluorescence (n = 122) on chemo-naive and postchemotherapy (post-CTX) resected patient samples (chemoradiotherapy excluded) to define the impact of neoadjuvant chemotherapy. Transcriptome analysis combined with high-resolution mapping of whole-tissue sections identified GATA6 (classical), KRT17 (basal-like) and cytochrome P450 3A (CYP3A) coexpressing cells that were preferentially enriched in post-CTX resected samples. The persistence of GATA6
    MeSH term(s) Humans ; Neoadjuvant Therapy ; Cytochrome P-450 CYP3A ; Adenocarcinoma ; Adjuvants, Immunologic ; Keratin-17 ; Phenotype
    Chemical Substances Cytochrome P-450 CYP3A (EC 1.14.14.1) ; Adjuvants, Immunologic ; Keratin-17
    Language English
    Publishing date 2023-09-07
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 2662-1347
    ISSN (online) 2662-1347
    DOI 10.1038/s43018-023-00628-6
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  10. Article ; Online: Phytotherapeutics oridonin and ponicidin show additive effects combined with irradiation in pancreatic cancer in vitro

    Liermann Jakob / Naumann Patrick / Fortunato Franco / Schmid Thomas E. / Weber Klaus-Josef / Debus Jürgen / Combs Stephanie E.

    Radiology and Oncology, Vol 51, Iss 4, Pp 407-

    2017  Volume 414

    Abstract: Chemoradiation of locally advanced non-metastatic pancreatic cancer can lead to secondary operability by tumor mass reduction. Here, we analyzed radiomodulating effects of oridonin and ponicidin in pancreatic cancer in vitro. Both agents are ent-kaurane ... ...

    Abstract Chemoradiation of locally advanced non-metastatic pancreatic cancer can lead to secondary operability by tumor mass reduction. Here, we analyzed radiomodulating effects of oridonin and ponicidin in pancreatic cancer in vitro. Both agents are ent-kaurane diterpenoids, extracted from Isodon rubescens, a plant that is well known in Traditional Chinese Medicine. Cytotoxic effects have recently been shown in different tumor entities for both agents.
    Keywords oridonin ; ponicidin ; irradiation ; pancreatic cancer ; γh2ax ; radiosensitivity ; Medical physics. Medical radiology. Nuclear medicine ; R895-920
    Language English
    Publishing date 2017-11-01T00:00:00Z
    Publisher Sciendo
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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