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  1. Artikel ; Online: Tumor Explants Elucidate a Cascade of Paracrine SHH, WNT, and VEGF Signals Driving Pancreatic Cancer Angiosuppression.

    Hasselluhn, Marie C / Decker-Farrell, Amanda R / Vlahos, Lukas / Thomas, Dafydd H / Curiel-Garcia, Alvaro / Maurer, H Carlo / Wasko, Urszula N / Tomassoni, Lorenzo / Sastra, Stephen A / Palermo, Carmine F / Dalton, Tanner C / Ma, Alice / Li, Fangda / Tolosa, Ezequiel J / Hibshoosh, Hanina / Fernandez-Zapico, Martin E / Muir, Alexander / Califano, Andrea / Olive, Kenneth P

    Cancer discovery

    2023  Band 14, Heft 2, Seite(n) 348–361

    Abstract: The sparse vascularity of pancreatic ductal adenocarcinoma (PDAC) presents a mystery: What prevents this aggressive malignancy from undergoing neoangiogenesis to counteract hypoxia and better support growth? An incidental finding from prior work on ... ...

    Abstract The sparse vascularity of pancreatic ductal adenocarcinoma (PDAC) presents a mystery: What prevents this aggressive malignancy from undergoing neoangiogenesis to counteract hypoxia and better support growth? An incidental finding from prior work on paracrine communication between malignant PDAC cells and fibroblasts revealed that inhibition of the Hedgehog (HH) pathway partially relieved angiosuppression, increasing tumor vascularity through unknown mechanisms. Initial efforts to study this phenotype were hindered by difficulties replicating the complex interactions of multiple cell types in vitro. Here we identify a cascade of paracrine signals between multiple cell types that act sequentially to suppress angiogenesis in PDAC. Malignant epithelial cells promote HH signaling in fibroblasts, leading to inhibition of noncanonical WNT signaling in fibroblasts and epithelial cells, thereby limiting VEGFR2-dependent activation of endothelial hypersprouting. This cascade was elucidated using human and murine PDAC explant models, which effectively retain the complex cellular interactions of native tumor tissues.
    Significance: We present a key mechanism of tumor angiosuppression, a process that sculpts the physiologic, cellular, and metabolic environment of PDAC. We further present a computational and experimental framework for the dissection of complex signaling cascades that propagate among multiple cell types in the tissue environment. This article is featured in Selected Articles from This Issue, p. 201.
    Mesh-Begriff(e) Animals ; Humans ; Mice ; Carcinoma, Pancreatic Ductal/pathology ; Cell Line, Tumor ; Cell Proliferation ; Hedgehog Proteins/genetics ; Pancreatic Neoplasms/pathology ; Vascular Endothelial Growth Factor A
    Chemische Substanzen Hedgehog Proteins ; SHH protein, human ; Vascular Endothelial Growth Factor A ; Shh protein, mouse ; VEGFA protein, human ; vascular endothelial growth factor A, mouse
    Sprache Englisch
    Erscheinungsdatum 2023-11-14
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 2625242-9
    ISSN 2159-8290 ; 2159-8274
    ISSN (online) 2159-8290
    ISSN 2159-8274
    DOI 10.1158/2159-8290.CD-23-0240
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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    Verfügbar in ZB MED Köln/Königswinter

    Zs.A 6916: Hefte anzeigen Standort:
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  2. Artikel ; Online: Tumour-selective activity of RAS-GTP inhibition in pancreatic cancer.

    Wasko, Urszula N / Jiang, Jingjing / Dalton, Tanner C / Curiel-Garcia, Alvaro / Edwards, A Cole / Wang, Yingyun / Lee, Bianca / Orlen, Margo / Tian, Sha / Stalnecker, Clint A / Drizyte-Miller, Kristina / Menard, Marie / Dilly, Julien / Sastra, Stephen A / Palermo, Carmine F / Hasselluhn, Marie C / Decker-Farrell, Amanda R / Chang, Stephanie / Jiang, Lingyan /
    Wei, Xing / Yang, Yu C / Helland, Ciara / Courtney, Haley / Gindin, Yevgeniy / Muonio, Karl / Zhao, Ruiping / Kemp, Samantha B / Clendenin, Cynthia / Sor, Rina / Vostrejs, William P / Hibshman, Priya S / Amparo, Amber M / Hennessey, Connor / Rees, Matthew G / Ronan, Melissa M / Roth, Jennifer A / Brodbeck, Jens / Tomassoni, Lorenzo / Bakir, Basil / Socci, Nicholas D / Herring, Laura E / Barker, Natalie K / Wang, Junning / Cleary, James M / Wolpin, Brian M / Chabot, John A / Kluger, Michael D / Manji, Gulam A / Tsai, Kenneth Y / Sekulic, Miroslav / Lagana, Stephen M / Califano, Andrea / Quintana, Elsa / Wang, Zhengping / Smith, Jacqueline A M / Holderfield, Matthew / Wildes, David / Lowe, Scott W / Badgley, Michael A / Aguirre, Andrew J / Vonderheide, Robert H / Stanger, Ben Z / Baslan, Timour / Der, Channing J / Singh, Mallika / Olive, Kenneth P

    Nature

    2024  Band 629, Heft 8013, Seite(n) 927–936

    Abstract: Broad-spectrum RAS inhibition has the potential to benefit roughly a quarter of human patients with cancer whose tumours are driven by RAS ... ...

    Abstract Broad-spectrum RAS inhibition has the potential to benefit roughly a quarter of human patients with cancer whose tumours are driven by RAS mutations
    Mesh-Begriff(e) Animals ; Pancreatic Neoplasms/drug therapy ; Pancreatic Neoplasms/pathology ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/metabolism ; Mice ; Humans ; Apoptosis/drug effects ; Cell Line, Tumor ; Carcinoma, Pancreatic Ductal/drug therapy ; Carcinoma, Pancreatic Ductal/pathology ; Carcinoma, Pancreatic Ductal/genetics ; Carcinoma, Pancreatic Ductal/metabolism ; Female ; Cell Proliferation/drug effects ; Guanosine Triphosphate/metabolism ; Disease Models, Animal ; Male ; ras Proteins/metabolism ; ras Proteins/antagonists & inhibitors ; ras Proteins/genetics ; Proto-Oncogene Proteins p21(ras)/genetics ; Proto-Oncogene Proteins p21(ras)/metabolism ; Proto-Oncogene Proteins p21(ras)/antagonists & inhibitors ; Neoplasm Recurrence, Local/drug therapy ; Neoplasm Recurrence, Local/genetics ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Xenograft Model Antitumor Assays
    Chemische Substanzen Guanosine Triphosphate (86-01-1) ; ras Proteins (EC 3.6.5.2) ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2) ; Antineoplastic Agents
    Sprache Englisch
    Erscheinungsdatum 2024-04-08
    Erscheinungsland England
    Dokumenttyp Journal Article
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/s41586-024-07379-z
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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    Verfügbar in ZB MED Köln/Königswinter

    Zs.A 26: Hefte anzeigen Standort:
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    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
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    Zs.MG 9: Hefte anzeigen
    Zs.MO 244: Hefte anzeigen

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