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  1. Article ; Online: Targeting menin: a promising therapeutic strategy for susceptible acute leukemia subtypes.

    Di Fazio, Pietro

    Signal transduction and targeted therapy

    2023  Volume 8, Issue 1, Page(s) 384

    MeSH term(s) Humans ; Leukemia, Myeloid, Acute/drug therapy ; Leukemia, Myeloid, Acute/genetics
    Language English
    Publishing date 2023-10-11
    Publishing country England
    Document type Journal Article
    ZDB-ID 2886872-9
    ISSN 2059-3635 ; 2095-9907
    ISSN (online) 2059-3635
    ISSN 2095-9907
    DOI 10.1038/s41392-023-01627-w
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  2. Article ; Online: The epitranscriptome: At the crossroad of cancer prognosis.

    Di Fazio, Pietro

    EBioMedicine

    2021  Volume 64, Page(s) 103231

    MeSH term(s) DNA Methylation ; Epigenesis, Genetic ; Epigenomics/methods ; Gene Expression Regulation, Neoplastic ; Humans ; Neoplasms/diagnosis ; Neoplasms/genetics ; Neoplasms/mortality ; Transcriptome
    Language English
    Publishing date 2021-01-28
    Publishing country Netherlands
    Document type Editorial
    ZDB-ID 2851331-9
    ISSN 2352-3964
    ISSN (online) 2352-3964
    DOI 10.1016/j.ebiom.2021.103231
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 7090: Show issues Location:
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  3. Article ; Online: The Expression of Autophagy-Associated Genes Represents a Valid Footprint for Aggressive Pancreatic Neuroendocrine Neoplasms.

    Matrood, Sami / Melms, Leander Edwin / Bartsch, Detlef Klaus / Di Fazio, Pietro

    International journal of molecular sciences

    2023  Volume 24, Issue 4

    Abstract: Pancreatic neuroendocrine neoplasms (pNEN) are rare and heterogeneous tumors. Previous investigations have shown that autophagy can be a target for cancer therapy. This study aimed to determine the association between the expression of autophagy- ... ...

    Abstract Pancreatic neuroendocrine neoplasms (pNEN) are rare and heterogeneous tumors. Previous investigations have shown that autophagy can be a target for cancer therapy. This study aimed to determine the association between the expression of autophagy-associated gene transcripts and clinical parameters in pNEN. In total, 54 pNEN specimens were obtained from our human biobank. The patient characteristics were retrieved from the medical record. RT-qPCR was performed to assess the expression of the autophagic transcripts
    MeSH term(s) Humans ; Gastrinoma/genetics ; Insulinoma/genetics ; Neuroendocrine Tumors/diagnosis ; Neuroendocrine Tumors/genetics ; Neuroendocrine Tumors/pathology ; Pancreatic Neoplasms/diagnosis ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/pathology ; Autophagy/genetics
    Language English
    Publishing date 2023-02-11
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms24043636
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  4. Article: Osteogenic Effect of Pregabalin in Human Primary Mesenchymal Stem Cells, Osteoblasts, and Osteosarcoma Cells.

    Wagener, Nele / Di Fazio, Pietro / Böker, Kai Oliver / Matziolis, Georg

    Life (Basel, Switzerland)

    2022  Volume 12, Issue 4

    Abstract: Seventy million patients worldwide are suffering from epilepsy. The long-term use of antiepileptic drugs causes the alteration of the bone tissue and its metabolism, thus increasing the risk of fractures. Clinical and pre-clinical studies have ... ...

    Abstract Seventy million patients worldwide are suffering from epilepsy. The long-term use of antiepileptic drugs causes the alteration of the bone tissue and its metabolism, thus increasing the risk of fractures. Clinical and pre-clinical studies have highlighted conflicting data on the influence of the relatively new antiepileptic drug pregabalin (Lyrica
    Language English
    Publishing date 2022-03-28
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2662250-6
    ISSN 2075-1729
    ISSN 2075-1729
    DOI 10.3390/life12040496
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  5. Article ; Online: HDACs as an emerging target in endocrine tumors: a comprehensive review.

    Klieser, Eckhard / Neumayer, Bettina / Di Fazio, Pietro / Mayr, Christian / Neureiter, Daniel / Kiesslich, Tobias

    Expert review of endocrinology & metabolism

    2023  Volume 18, Issue 2, Page(s) 143–154

    Abstract: Introduction: The pathogenic role of deregulated histone (de-)acetylation by histone deacetyles (HDACs) has been demonstrated in several human cancers. While some HDAC inhibitors (HDACi) have been approved for individual entities, for endocrine tumors ... ...

    Abstract Introduction: The pathogenic role of deregulated histone (de-)acetylation by histone deacetyles (HDACs) has been demonstrated in several human cancers. While some HDAC inhibitors (HDACi) have been approved for individual entities, for endocrine tumors such translation into clinical practice has not yet been achieved.
    Areas covered: Relevant results identified by structured searches in PubMed as well as in reference lists are summarized in a narrative review to discuss the current knowledge of HDAC involvement and their therapeutic relevance in endocrine tumors. For thyroid, neuroendocrine, and adrenal tumors, various oncogenic mechanisms of HDAC deregulation and effects of HDAC inhibitors (HDACi) have been identified in preclinical studies including direct cancer cell toxicity and modification of differentiation status.
    Expert opinion: Based on positive pre-clinical results, the research on HDAC (inhibition) in the various endocrine tumors should be intensified - yet, it needs to be considered that i) HDACs' oncogenic actions might constitute only a part of epigenetic mechanisms driving cancer, ii) individual HDAC has different roles in different endocrine tumor entities, iii) inhibition of HDACs might be especially attractive in combination with conventional or other targeted therapies, and iv) new HDAC-inhibiting drugs with improved specificity or functionally modified HDACi might further improve their efficacy.
    MeSH term(s) Humans ; Histones/metabolism ; Histones/therapeutic use ; Histone Deacetylase Inhibitors/pharmacology ; Histone Deacetylase Inhibitors/therapeutic use ; Histone Deacetylases/genetics ; Histone Deacetylases/metabolism ; Histone Deacetylases/therapeutic use ; Neoplasms ; Epigenesis, Genetic
    Chemical Substances Histones ; Histone Deacetylase Inhibitors ; Histone Deacetylases (EC 3.5.1.98)
    Language English
    Publishing date 2023-03-06
    Publishing country England
    Document type Review ; Journal Article
    ISSN 1744-8417
    ISSN (online) 1744-8417
    DOI 10.1080/17446651.2023.2183840
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  6. Article: Targeting autophagy in liver cancer.

    Di Fazio, Pietro / Matrood, Sami

    Translational gastroenterology and hepatology

    2018  Volume 3, Page(s) 39

    Abstract: Autophagy is a catabolic cellular process conserved in animals. It is characterized by the main role of recycling all the non-functional products of the cells. Once, autophagy players detect non-functioning sub-cellular organelles and proteins, they ... ...

    Abstract Autophagy is a catabolic cellular process conserved in animals. It is characterized by the main role of recycling all the non-functional products of the cells. Once, autophagy players detect non-functioning sub-cellular organelles and proteins, they start the so-called nucleation process. The organelles will be surrounded by a double membrane vesicle mainly constituted by endoplasmic reticulum (ER) membrane and autophagy proteins, e.g., MAP1LC3B, Beclin-1, VPS34, Unc-51 like autophagy activating kinase (ULK1) and ubiquitination-related proteins. Then the autophagic membrane will go through an elongation phase involving additional autophagy players. Once the autophagic vesicle is complete, the sub-cellular organelles will be isolated from the rest of the cytosol and driven to the final fusion with lysosomes. Here, the digestion process will end. Alteration and or impairment of autophagy have been shown to be correlated with development of diseases affecting the central nervous system, e.g., Alzheimer and other neurodegenerative diseases. Nonetheless, autophagy defect is responsible for tumorigenesis in blood and solid malignancies, in particular liver cancer. Malignancies of the liver are determined by several genetics and epigenetics mechanisms triggering the up-regulation of survival mechanisms and resistance to cell death. Furthermore, liver cancer could result from pathologic conditions like cirrhosis and fibrosis related to virus infection, aflatoxin, alcohol consumption and high fat diet together with insulin resistance. The role exerted by autophagy in the pathogenesis of the liver and tumor development has been evidenced in recent years. The alteration of autophagy assumes a fundamental role for liver tumorigenesis determining an accumulation of non-functional proteins and organelles that trigger oxidative stress leading to genotoxic stress and gene alterations. Furthermore, the absence of this degradation mechanism could prompt the cells to alter their metabolic status and turn into malignant cells. Interestingly, the heterozygous loss of function of Beclin-1 is able to trigger liver tumorigenesis or even the simple accumulation of proteins caused by the block of the final autolysosome fusion and degradation process is responsible for liver cancer development. This review highlights the importance of targeting the autophagy process in liver cancer in order to restore its function and to promote autophagy-mediated cell demise.
    Language English
    Publishing date 2018-07-10
    Publishing country China
    Document type Journal Article ; Review
    ISSN 2415-1289
    ISSN 2415-1289
    DOI 10.21037/tgh.2018.06.09
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  7. Article: Chondral/Desmal Osteogenesis in 3D Spheroids Sensitized by Psychostimulants.

    Wagener, Nele / Lehmann, Wolfgang / Böker, Kai O / Röhner, Eric / Di Fazio, Pietro

    Journal of clinical medicine

    2022  Volume 11, Issue 20

    Abstract: Attention deficit hyperactivity disorder (ADHD) affects 6.4 million children in the United States of America. Children and adolescents, the main consumers of ADHD medication, are in the bone growth phase, which extends over a period of up to two decades. ...

    Abstract Attention deficit hyperactivity disorder (ADHD) affects 6.4 million children in the United States of America. Children and adolescents, the main consumers of ADHD medication, are in the bone growth phase, which extends over a period of up to two decades. Thus, impaired proliferation and maturation of chondrocytes and osteoblasts can result in impaired bone formation. The aim of this study is to investigate, for the first time, the effects of the ADHD-medication modafinil, atomoxetine and guanfacine on bone growth and repair in vitro. Using two-dimensional and three-dimensional cell models, we investigated the chondrogenic/osteogenic differentiation, proliferation and viability of human mesenchymal progenitor cells. Real-time cell proliferation was measured by xCELLigence. Live/dead staining and size measurement of hMSC- and MG63 monolayer and spheroids were performed after administration of therapeutic plasma concentrations of modafinil, atomoxetine and guanfacine. Chondrogenic differentiation was quantified by RTqPCR. The chondrogenic and osteogenic differentiation was evaluated by histological cryo-sections. Modafinil, atomoxetine and guanfacine reduced chondrogenic and osteogenic differentiation terms of transcript expression and at the histological level. Cell viability of the MG63- and hMSC monolayer was not impeded by ADHD-medication. Our in vitro results indicate that modafinil, atomoxetine and guanfacine may impair chondrogenic and osteogenic differentiation in a 3D model reflecting the in vivo physiologic condition.
    Language English
    Publishing date 2022-10-21
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2662592-1
    ISSN 2077-0383
    ISSN 2077-0383
    DOI 10.3390/jcm11206218
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  8. Article: Whole-exome sequencing of calcitonin-producing pancreatic neuroendocrine neoplasms indicates a unique molecular signature.

    Döring, Claudia / Peer, Katharina / Bankov, Katrin / Bollmann, Carmen / Ramaswamy, Annette / Di Fazio, Pietro / Wild, Peter Johannes / Bartsch, Detlef Klaus

    Frontiers in oncology

    2023  Volume 13, Page(s) 1160921

    Abstract: Introduction: Calcitonin-producing pancreatic neuroendocrine neoplasms (CT-pNENs) are an extremely rare clinical entity, with approximately 60 cases reported worldwide. While CT-pNENs can mimic the clinical and diagnostic features of medullary thyroid ... ...

    Abstract Introduction: Calcitonin-producing pancreatic neuroendocrine neoplasms (CT-pNENs) are an extremely rare clinical entity, with approximately 60 cases reported worldwide. While CT-pNENs can mimic the clinical and diagnostic features of medullary thyroid carcinoma, their molecular profile is poorly understood.
    Methods: Whole-exome sequencing (WES) was performed on tumor and corresponding serum samples of five patients with increased calcitonin serum levels and histologically validated calcitonin-positive CT-pNENs. cBioPortal analysis and DAVID gene enrichment analysis were performed to identify dysregulated candidate genes compared to control databases. Immunohistochemistry was used to detect the protein expression of
    Results: Mutated genes known in the literature in pNENs like
    Discussion: CT-pNENs have a unique molecular signature compared to other pNEN subtypes, specifically involving the
    Language English
    Publishing date 2023-09-12
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2649216-7
    ISSN 2234-943X
    ISSN 2234-943X
    DOI 10.3389/fonc.2023.1160921
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  9. Article: Toll-like receptor 5 tunes hepatic and pancreatic stellate cells activation.

    Di Fazio, Pietro / Mielke, Sophia / Böhm, Isabell T / Buchholz, Malte / Matrood, Sami / Schuppan, Detlef / Wissniowski, Thaddeus

    BMJ open gastroenterology

    2023  Volume 10, Issue 1

    Abstract: Objective: Stellate cells are responsible for liver and pancreas fibrosis and strictly correlate with tumourigenesis. Although their activation is reversible, an exacerbated signalling triggers chronic fibrosis. Toll-like receptors (TLRs) modulate ... ...

    Abstract Objective: Stellate cells are responsible for liver and pancreas fibrosis and strictly correlate with tumourigenesis. Although their activation is reversible, an exacerbated signalling triggers chronic fibrosis. Toll-like receptors (TLRs) modulate stellate cells transition. TLR5 transduces the signal deriving by the binding to bacterial flagellin from invading mobile bacteria.
    Design: Human hepatic and pancreatic stellate cells were activated by the administration of transforming growth factor-beta (TGF-β). TLR5 was transiently knocked down by short-interference RNA transfection. Reverse Transcription-quantitativePCR and western blot were performed to analyse the transcript and protein level of TLR5 and the transition players. Fluorescence microscopy was performed to identify these targets in spheroids and in the sections of murine fibrotic liver.
    Results: TGF-β-activated human hepatic and pancreatic stellate cells showed an increase of
    Conclusion: TGF-β-mediated activation of hepatic and pancreatic stellate cells requires the over-expression of TLR5. Instead, its autonomous signalling inhibits the activation of the stellate cells, thus prompting a signalling through different regulatory pathways.
    MeSH term(s) Animals ; Humans ; Mice ; Flagellin/pharmacology ; Liver Cirrhosis ; Pancreatic Stellate Cells ; Toll-Like Receptor 5/metabolism
    Chemical Substances Flagellin (12777-81-0) ; Toll-Like Receptor 5 ; TLR5 protein, human ; Tlr5 protein, mouse
    Language English
    Publishing date 2023-07-11
    Publishing country England
    Document type Journal Article
    ISSN 2054-4774
    ISSN 2054-4774
    DOI 10.1136/bmjgast-2023-001148
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  10. Article ; Online: Synergic Induction of Autophagic Cell Death in Anaplastic Thyroid Carcinoma.

    Wächter, Sabine / Knauff, Franziska / Roth, Silvia / Keber, Corinna / Holzer, Katharina / Manoharan, Jerena / Maurer, Elisabeth / Bartsch, Detlef K / Di Fazio, Pietro

    Cancer investigation

    2023  Volume 41, Issue 4, Page(s) 405–421

    Abstract: Anaplastic thyroid carcinoma (ATC) has poor prognosis, high mortality rate and lack of effective therapy. A synergic combination of PD-L1 antibody together with cell death promoting substances like deacetylase inhibitors (DACi) and multi-kinase ... ...

    Abstract Anaplastic thyroid carcinoma (ATC) has poor prognosis, high mortality rate and lack of effective therapy. A synergic combination of PD-L1 antibody together with cell death promoting substances like deacetylase inhibitors (DACi) and multi-kinase inhibitors (MKI) could sensitize ATC cells and promote decay by autophagic cell death. The PD-L1-inhibitor atezolizumab synergized with panobinostat (DACi) and sorafenib (MKI) leading to significant reduction of the viability, measured by real time luminescence, of three different patient-derived primary ATC cells, of C643 cells and follicular epithelial thyroid cells too.
    MeSH term(s) Autophagy ; Thyroid Carcinoma, Anaplastic/drug therapy ; Thyroid Carcinoma, Anaplastic/pathology ; Thyroid Neoplasms/drug therapy ; Thyroid Neoplasms/pathology ; Panobinostat/pharmacology ; Sorafenib/pharmacology ; Cell Line, Tumor ; Antineoplastic Agents/pharmacology ; Humans ; Male ; Aged ; Aged, 80 and over ; Cell Death ; Spheroids, Cellular
    Chemical Substances atezolizumab (52CMI0WC3Y) ; Panobinostat (9647FM7Y3Z) ; Sorafenib (9ZOQ3TZI87) ; Antineoplastic Agents
    Language English
    Publishing date 2023-03-01
    Publishing country England
    Document type Journal Article
    ZDB-ID 604942-4
    ISSN 1532-4192 ; 0735-7907
    ISSN (online) 1532-4192
    ISSN 0735-7907
    DOI 10.1080/07357907.2023.2183027
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    In stock of ZB MED Cologne/Königswinter

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