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  1. Article: Tuft cells transdifferentiate to neural-like progenitor cells in the progression of pancreatic cancer.

    Salas-Escabillas, Daniel J / Hoffman, Megan T / Moore, Jacee S / Brender, Sydney M / Wen, Hui-Ju / Benitz, Simone / Davis, Erick T / Long, Dan / Wombwell, Allison M / Steele, Nina G / Sears, Rosalie C / Matsumoto, Ichiro / DelGiorno, Kathleen E / Crawford, Howard C

    bioRxiv : the preprint server for biology

    2024  

    Abstract: Pancreatic ductal adenocarcinoma (PDA) is partly initiated through the transdifferentiation of acinar cells to metaplastic ducts that act as precursors of neoplasia and cancer. Tuft cells are solitary chemosensory cells not found in the normal pancreas ... ...

    Abstract Pancreatic ductal adenocarcinoma (PDA) is partly initiated through the transdifferentiation of acinar cells to metaplastic ducts that act as precursors of neoplasia and cancer. Tuft cells are solitary chemosensory cells not found in the normal pancreas but arise in metaplasia and neoplasia, diminishing as neoplastic lesions progress to carcinoma. Metaplastic tuft cells (mTCs) function to suppress tumor progression through communication with the tumor microenvironment, but their fate during progression is unknown. To determine the fate of mTCs during PDA progression, we have created a lineage tracing model that uses a tamoxifen-inducible tuft-cell specific Pou2f3
    Language English
    Publishing date 2024-04-23
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2024.02.12.579982
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: ROR2 regulates cellular plasticity in pancreatic neoplasia and adenocarcinoma.

    Benitz, Simone / Steep, Alec / Nasser, Malak / Preall, Jonathan / Mahajan, Ujjwal M / McQuithey, Holly / Loveless, Ian / Davis, Erick T / Wen, Hui-Ju / Long, Daniel W / Metzler, Thomas / Zwernik, Samuel / Louw, Michaela / Rempinski, Donald / Salas-Escabillas, Daniel / Brender, Sydney / Song, Linghao / Huang, Ling / Zhang, Zhenyu /
    Steele, Nina G / Regel, Ivonne / Bednar, Filip / Crawford, Howard C

    bioRxiv : the preprint server for biology

    2024  

    Abstract: Cellular plasticity is a hallmark of pancreatic ductal adenocarcinoma (PDAC) starting from the conversion of normal cells into precancerous lesions to the progression of carcinoma subtypes associated with aggressiveness and therapeutic response. We ... ...

    Abstract Cellular plasticity is a hallmark of pancreatic ductal adenocarcinoma (PDAC) starting from the conversion of normal cells into precancerous lesions to the progression of carcinoma subtypes associated with aggressiveness and therapeutic response. We discovered that normal acinar cell differentiation, maintained by the transcription factor Pdx1, suppresses a broad gastric cell identity that is maintained in metaplasia, neoplasia, and the classical subtype of PDAC in mouse and human. We have identified the receptor tyrosine kinase Ror2 as marker of a gastric metaplasia (SPEM)-like identity in the pancreas. Ablation of
    Language English
    Publishing date 2024-01-16
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.12.13.571566
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Arginase 1 is a key driver of immune suppression in pancreatic cancer.

    Menjivar, Rosa E / Nwosu, Zeribe C / Du, Wenting / Donahue, Katelyn L / Hong, Hanna S / Espinoza, Carlos / Brown, Kristee / Velez-Delgado, Ashley / Yan, Wei / Lima, Fatima / Bischoff, Allison / Kadiyala, Padma / Salas-Escabillas, Daniel / Crawford, Howard C / Bednar, Filip / Carpenter, Eileen / Zhang, Yaqing / Halbrook, Christopher J / Lyssiotis, Costas A /
    Pasca di Magliano, Marina

    eLife

    2023  Volume 12

    Abstract: An extensive fibroinflammatory stroma rich in macrophages is a hallmark of pancreatic cancer. In this disease, it is well appreciated that macrophages are immunosuppressive and contribute to the poor response to immunotherapy; however, the mechanisms of ... ...

    Abstract An extensive fibroinflammatory stroma rich in macrophages is a hallmark of pancreatic cancer. In this disease, it is well appreciated that macrophages are immunosuppressive and contribute to the poor response to immunotherapy; however, the mechanisms of immune suppression are complex and not fully understood. Immunosuppressive macrophages are classically defined by the expression of the enzyme Arginase 1 (ARG1), which we demonstrated is potently expressed in pancreatic tumor-associated macrophages from both human patients and mouse models. While routinely used as a polarization marker, ARG1 also catabolizes arginine, an amino acid required for T cell activation and proliferation. To investigate this metabolic function, we used a genetic and a pharmacologic approach to target
    MeSH term(s) Animals ; Humans ; Mice ; Arginase/genetics ; Arginase/metabolism ; Arginine/metabolism ; CD8-Positive T-Lymphocytes ; Macrophages ; Pancreatic Neoplasms/pathology
    Chemical Substances Arginase (EC 3.5.3.1) ; Arginine (94ZLA3W45F) ; Arg1 protein, mouse (EC 3.5.3.1) ; ARG1 protein, human (EC 3.5.3.1)
    Language English
    Publishing date 2023-02-02
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2687154-3
    ISSN 2050-084X ; 2050-084X
    ISSN (online) 2050-084X
    ISSN 2050-084X
    DOI 10.7554/eLife.80721
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Combinatorial Gli activity directs immune infiltration and tumor growth in pancreatic cancer.

    Scales, Michael K / Velez-Delgado, Ashley / Steele, Nina G / Schrader, Hannah E / Stabnick, Anna M / Yan, Wei / Mercado Soto, Nayanna M / Nwosu, Zeribe C / Johnson, Craig / Zhang, Yaqing / Salas-Escabillas, Daniel J / Menjivar, Rosa E / Maurer, H Carlo / Crawford, Howard C / Bednar, Filip / Olive, Kenneth P / Pasca di Magliano, Marina / Allen, Benjamin L

    PLoS genetics

    2022  Volume 18, Issue 7, Page(s) e1010315

    Abstract: Proper Hedgehog (HH) signaling is essential for embryonic development, while aberrant HH signaling drives pediatric and adult cancers. HH signaling is frequently dysregulated in pancreatic cancer, yet its role remains controversial, with both tumor- ... ...

    Abstract Proper Hedgehog (HH) signaling is essential for embryonic development, while aberrant HH signaling drives pediatric and adult cancers. HH signaling is frequently dysregulated in pancreatic cancer, yet its role remains controversial, with both tumor-promoting and tumor-restraining functions reported. Notably, the GLI family of HH transcription factors (GLI1, GLI2, GLI3), remain largely unexplored in pancreatic cancer. We therefore investigated the individual and combined contributions of GLI1-3 to pancreatic cancer progression. At pre-cancerous stages, fibroblast-specific Gli2/Gli3 deletion decreases immunosuppressive macrophage infiltration and promotes T cell infiltration. Strikingly, combined loss of Gli1/Gli2/Gli3 promotes macrophage infiltration, indicating that subtle changes in Gli expression differentially regulate immune infiltration. In invasive tumors, Gli2/Gli3 KO fibroblasts exclude immunosuppressive myeloid cells and suppress tumor growth by recruiting natural killer cells. Finally, we demonstrate that fibroblasts directly regulate macrophage and T cell migration through the expression of Gli-dependent cytokines. Thus, the coordinated activity of GLI1-3 directs the fibroinflammatory response throughout pancreatic cancer progression.
    MeSH term(s) Adult ; Child ; Female ; Hedgehog Proteins/genetics ; Hedgehog Proteins/metabolism ; Humans ; Kruppel-Like Transcription Factors/genetics ; Kruppel-Like Transcription Factors/metabolism ; Nerve Tissue Proteins/metabolism ; Pancreatic Neoplasms/genetics ; Pregnancy ; Zinc Finger Protein GLI1/genetics ; Zinc Finger Protein Gli2/genetics ; Zinc Finger Protein Gli3/genetics
    Chemical Substances Hedgehog Proteins ; Kruppel-Like Transcription Factors ; Nerve Tissue Proteins ; Zinc Finger Protein GLI1 ; Zinc Finger Protein Gli2 ; Zinc Finger Protein Gli3
    Language English
    Publishing date 2022-07-22
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2186725-2
    ISSN 1553-7404 ; 1553-7390
    ISSN (online) 1553-7404
    ISSN 1553-7390
    DOI 10.1371/journal.pgen.1010315
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: The Gustatory Sensory G-Protein GNAT3 Suppresses Pancreatic Cancer Progression in Mice.

    Hoffman, Megan T / Kemp, Samantha B / Salas-Escabillas, Daniel J / Zhang, Yaqing / Steele, Nina G / The, Stephanie / Long, Daniel / Benitz, Simone / Yan, Wei / Margolskee, Robert F / Bednar, Filip / Pasca di Magliano, Marina / Wen, Hui-Ju / Crawford, Howard C

    Cellular and molecular gastroenterology and hepatology

    2020  Volume 11, Issue 2, Page(s) 349–369

    Abstract: Background & aims: Pancreatic ductal adenocarcinoma (PDA) initiation and progression are accompanied by an immunosuppressive inflammatory response. Here, we evaluated the immunomodulatory role of chemosensory signaling in metaplastic tuft cells (MTCs) ... ...

    Abstract Background & aims: Pancreatic ductal adenocarcinoma (PDA) initiation and progression are accompanied by an immunosuppressive inflammatory response. Here, we evaluated the immunomodulatory role of chemosensory signaling in metaplastic tuft cells (MTCs) by analyzing the role of GNAT3, a gustatory pathway G-protein expressed by MTCs, during PDA progression.
    Methods: Gnat3-null (Gnat3
    Results: Ablation of Gnat3 in KC organoids increased release of tumor-promoting cytokines in conditioned media, including CXCL1 and CXCL2. Analysis of Gnat3
    Conclusions: Compromised gustatory sensing, achieved by Gnat3 ablation, enhanced the CXCL1/2-CXCR2 axis to alter the MDSC population and promoted the progression of metastatic PDA.
    MeSH term(s) Animals ; Carcinogenesis/immunology ; Carcinogenesis/pathology ; Carcinoma, Pancreatic Ductal/genetics ; Carcinoma, Pancreatic Ductal/immunology ; Carcinoma, Pancreatic Ductal/pathology ; Cells, Cultured ; Chemokine CXCL1/metabolism ; Chemokine CXCL2/metabolism ; Culture Media, Conditioned/metabolism ; Disease Models, Animal ; Heterotrimeric GTP-Binding Proteins/genetics ; Heterotrimeric GTP-Binding Proteins/metabolism ; Humans ; Mice ; Mice, Knockout ; Myeloid-Derived Suppressor Cells ; Organoids ; Pancreatic Ducts/immunology ; Pancreatic Ducts/pathology ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/immunology ; Pancreatic Neoplasms/pathology ; Primary Cell Culture ; Proto-Oncogene Proteins p21(ras)/genetics ; Signal Transduction/immunology
    Chemical Substances Chemokine CXCL1 ; Chemokine CXCL2 ; Culture Media, Conditioned ; Cxcl1 protein, mouse ; Cxcl2 protein, mouse ; GNAT3 protein, mouse (EC 3.6.5.1) ; Heterotrimeric GTP-Binding Proteins (EC 3.6.5.1) ; Hras protein, mouse (EC 3.6.5.2) ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2)
    Language English
    Publishing date 2020-08-31
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2819778-1
    ISSN 2352-345X ; 2352-345X
    ISSN (online) 2352-345X
    ISSN 2352-345X
    DOI 10.1016/j.jcmgh.2020.08.011
    Database MEDical Literature Analysis and Retrieval System OnLINE

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