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  1. AU="Pasini, Davide"
  2. AU="Barbieri, Magali"
  3. AU="Kanizsai, Péter"
  4. AU="Altahawi, Faysal" AU="Altahawi, Faysal"
  5. AU="Rai, Anurag"
  6. AU="Udrea, Ana Maria"
  7. AU=Lo Giudice Roberto

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  1. Artikel ; Online: Axon guidance cue SEMA3A promotes the aggressive phenotype of basal-like PDAC.

    Lupo, Francesca / Pezzini, Francesco / Pasini, Davide / Fiorini, Elena / Adamo, Annalisa / Veghini, Lisa / Bevere, Michele / Frusteri, Cristina / Delfino, Pietro / D'agosto, Sabrina / Andreani, Silvia / Piro, Geny / Malinova, Antonia / Wang, Tian / De Sanctis, Francesco / Lawlor, Rita Teresa / Hwang, Chang-Il / Carbone, Carmine / Amelio, Ivano /
    Bailey, Peter / Bronte, Vincenzo / Tuveson, David / Scarpa, Aldo / Ugel, Stefano / Corbo, Vincenzo

    Gut

    2024  

    Abstract: Objective: The dysregulation of the axon guidance pathway is common in pancreatic ductal adenocarcinoma (PDAC), yet our understanding of its biological relevance is limited. Here, we investigated the functional role of the axon guidance cue SEMA3A in ... ...

    Abstract Objective: The dysregulation of the axon guidance pathway is common in pancreatic ductal adenocarcinoma (PDAC), yet our understanding of its biological relevance is limited. Here, we investigated the functional role of the axon guidance cue SEMA3A in supporting PDAC progression.
    Design: We integrated bulk and single-cell transcriptomic datasets of human PDAC with in situ hybridisation analyses of patients' tissues to evaluate SEMA3A expression in molecular subtypes of PDAC. Gain and loss of function experiments in PDAC cell lines and organoids were performed to dissect how SEMA3A contributes to define a biologically aggressive phenotype.
    Results: In PDAC tissues, SEMA3A is expressed by stromal elements and selectively enriched in basal-like/squamous epithelial cells. Accordingly, expression of SEMA3A in PDAC cells is induced by both cell-intrinsic and cell-extrinsic determinants of the basal-like phenotype.
    Conclusions: Here, we show that SEMA3A is a stress-sensitive locus that promotes the malignant phenotype of basal-like PDAC through both cell-intrinsic and cell-extrinsic mechanisms.
    Sprache Englisch
    Erscheinungsdatum 2024-04-26
    Erscheinungsland England
    Dokumenttyp Journal Article
    ZDB-ID 80128-8
    ISSN 1468-3288 ; 0017-5749
    ISSN (online) 1468-3288
    ISSN 0017-5749
    DOI 10.1136/gutjnl-2023-329807
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Assessing Biocompatibility of Face Mask Materials during COVID-19 Pandemic by a Rapid Multi-Assays Strategy.

    Petrachi, Tiziana / Ganzerli, Francesco / Cuoghi, Aurora / Ferrari, Alberto / Resca, Elisa / Bergamini, Valentina / Accorsi, Luca / Burini, Francesco / Pasini, Davide / Arnaud, Gaelle Françoise / Piccini, Mattia / Aldrovandi, Laura / Mari, Giorgio / Tomasi, Aldo / Rovati, Luigi / Dominici, Massimo / Veronesi, Elena

    International journal of environmental research and public health

    2021  Band 18, Heft 10

    Abstract: During the coronavirus disease 2019 (COVID-19) pandemic, scientific authorities strongly suggested the use of face masks (FMs). FM materials (FMMs) have to satisfy the medical device biocompatibility requirements as indicated in the technical standard EN ...

    Abstract During the coronavirus disease 2019 (COVID-19) pandemic, scientific authorities strongly suggested the use of face masks (FMs). FM materials (FMMs) have to satisfy the medical device biocompatibility requirements as indicated in the technical standard EN ISO 10993-1:2018. The biologic evaluation must be confirmed by in vivo tests to verify cytotoxicity, sensitisation, and skin irritation. Some of these tests require an extensive period of time for their execution, which is incompatible with an emergency situation. In this study, we propose to verify the safety of FMMs combining the assessment of 3-[4,5-dimethylthiazolyl-2]-2,5-diphenyltetrazolium bromide (MTT) with quantification of nitric oxide (NO) and interleukin-6 (IL-6), as predictive markers of skin sensitisation or irritation based on human primary fibroblasts. Two hundred and forty-two FMMs were collected and classified according to spectrometer IR in polypropylene, paper, cotton, polyester, polyethylene terephthalate, 3-dimensional printing, and viscose. Of all FMMs tested, 50.8% passed all the assays, 48% failed at least one, and only 1.2% failed all. By a low cost, rapid and highly sensitive multi assays strategy tested on human skin fibroblasts against a large variety of FMMs, we propose a strategy to promptly evaluate biocompatibility in wearable materials.
    Mesh-Begriff(e) COVID-19 ; Humans ; Masks ; Pandemics ; SARS-CoV-2 ; Textiles
    Sprache Englisch
    Erscheinungsdatum 2021-05-18
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1660-4601
    ISSN (online) 1660-4601
    DOI 10.3390/ijerph18105387
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: Loss of FGFR4 promotes the malignant phenotype of PDAC.

    D'Agosto, Sabrina / Pezzini, Francesco / Veghini, Lisa / Delfino, Pietro / Fiorini, Claudia / Temgue Tane, Gael D / Del Curatolo, Anais / Vicentini, Caterina / Ferrari, Giorgia / Pasini, Davide / Andreani, Silvia / Lupo, Francesca / Fiorini, Elena / Lorenzon, Giulia / Lawlor, Rita T / Rusev, Borislav / Malinova, Antonia / Luchini, Claudio / Milella, Michele /
    Sereni, Elisabetta / Pea, Antonio / Bassi, Claudio / Bailey, Peter / Scarpa, Aldo / Bria, Emilio / Corbo, Vincenzo

    Oncogene

    2022  Band 41, Heft 38, Seite(n) 4371–4384

    Abstract: Transcriptomic analyses of pancreatic ductal adenocarcinoma (PDAC) have identified two major epithelial subtypes with distinct biology and clinical behaviours. Here, we aimed to clarify the role of FGFR1 and FGFR4 in the definition of aggressive PDAC ... ...

    Abstract Transcriptomic analyses of pancreatic ductal adenocarcinoma (PDAC) have identified two major epithelial subtypes with distinct biology and clinical behaviours. Here, we aimed to clarify the role of FGFR1 and FGFR4 in the definition of aggressive PDAC phenotypes. We found that the expression of FGFR4 is exclusively detected in epithelial cells, significantly elevated in the classical PDAC subtype, and associates with better outcomes. In highly aggressive basal-like/squamous PDAC, reduced FGFR4 expression aligns with hypermethylation of the gene and lower levels of histone marks associated with active transcription in its regulatory regions. Conversely, FGFR1 has more promiscuous expression in both normal and malignant pancreatic tissues and is strongly associated with the EMT phenotype but not with the basal-like cell lineage. Regardless of the genetic background, the increased proliferation of FGFR4-depleted PDAC cells correlates with hyperactivation of the mTORC1 pathway both in vitro and in vivo. Downregulation of FGFR4 in classical cell lines invariably leads to the enrichment of basal-like/squamous gene programs and is associated with either partial or full switch of phenotype. In sum, we show that endogenous levels of FGFR4 limit the malignant phenotype of PDAC cells. Finally, we propose FGFR4 as a valuable marker for the stratification of PDAC patients.
    Mesh-Begriff(e) Carcinoma, Pancreatic Ductal/pathology ; Carcinoma, Squamous Cell ; Humans ; Mechanistic Target of Rapamycin Complex 1/genetics ; Pancreatic Neoplasms/pathology ; Phenotype ; Receptor, Fibroblast Growth Factor, Type 4/genetics ; Pancreatic Neoplasms
    Chemische Substanzen FGFR4 protein, human (EC 2.7.10.1) ; Receptor, Fibroblast Growth Factor, Type 4 (EC 2.7.10.1) ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1)
    Sprache Englisch
    Erscheinungsdatum 2022-08-13
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 639046-8
    ISSN 1476-5594 ; 0950-9232
    ISSN (online) 1476-5594
    ISSN 0950-9232
    DOI 10.1038/s41388-022-02432-5
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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