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  1. Article ; Online: UCP2 and pancreatic cancer: conscious uncoupling for therapeutic effect.

    Caggiano, Emily G / Taniguchi, Cullen M

    Cancer metastasis reviews

    2024  

    Abstract: Pancreatic cancer has an exaggerated dependence on mitochondrial metabolism, but methods to specifically target the mitochondria without off target effects in normal tissues that rely on these organelles is a significant challenge. The mitochondrial ... ...

    Abstract Pancreatic cancer has an exaggerated dependence on mitochondrial metabolism, but methods to specifically target the mitochondria without off target effects in normal tissues that rely on these organelles is a significant challenge. The mitochondrial uncoupling protein 2 (UCP2) has potential as a cancer-specific drug target, and thus, we will review the known biology of UCP2 and discuss its potential role in the pathobiology and future therapy of pancreatic cancer.
    Language English
    Publishing date 2024-01-09
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 604857-2
    ISSN 1573-7233 ; 0167-7659
    ISSN (online) 1573-7233
    ISSN 0167-7659
    DOI 10.1007/s10555-023-10157-4
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1812: Show issues Location:
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    Jg. 1995 - 2021: Lesesall (1.OG)
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  2. Article ; Online: Mesenchymal and stem-like prostate cancer linked to therapy-induced lineage plasticity and metastasis.

    Han, Hyunho / Wang, Yan / Curto, Josue / Gurrapu, Sreeharsha / Laudato, Sara / Rumandla, Alekya / Chakraborty, Goutam / Wang, Xiaobo / Chen, Hong / Jiang, Yan / Kumar, Dhiraj / Caggiano, Emily G / Capogiri, Monica / Zhang, Boyu / Ji, Yan / Maity, Sankar N / Hu, Min / Bai, Shanshan / Aparicio, Ana M /
    Efstathiou, Eleni / Logothetis, Christopher J / Navin, Nicholas / Navone, Nora M / Chen, Yu / Giancotti, Filippo G

    Cell reports

    2022  Volume 39, Issue 1, Page(s) 110595

    Abstract: Bioinformatic analysis of 94 patient-derived xenografts (PDXs), cell lines, and organoids (PCOs) identifies three intrinsic transcriptional subtypes of metastatic castration-resistant prostate cancer: androgen receptor (AR) pathway + prostate cancer (PC) ...

    Abstract Bioinformatic analysis of 94 patient-derived xenografts (PDXs), cell lines, and organoids (PCOs) identifies three intrinsic transcriptional subtypes of metastatic castration-resistant prostate cancer: androgen receptor (AR) pathway + prostate cancer (PC) (ARPC), mesenchymal and stem-like PC (MSPC), and neuroendocrine PC (NEPC). A sizable proportion of castration-resistant and metastatic stage PC (M-CRPC) cases are admixtures of ARPC and MSPC. Analysis of clinical datasets and mechanistic studies indicates that MSPC arises from ARPC as a consequence of therapy-induced lineage plasticity. AR blockade with enzalutamide induces (1) transcriptional silencing of TP53 and hence dedifferentiation to a hybrid epithelial and mesenchymal and stem-like state and (2) inhibition of BMP signaling, which promotes resistance to AR inhibition. Enzalutamide-tolerant LNCaP cells re-enter the cell cycle in response to neuregulin and generate metastasis in mice. Combined inhibition of HER2/3 and AR or mTORC1 exhibits efficacy in models of ARPC and MSPC or MSPC, respectively. These results define MSPC, trace its origin to therapy-induced lineage plasticity, and reveal its sensitivity to HER2/3 inhibition.
    MeSH term(s) Animals ; Antineoplastic Agents/pharmacology ; Benzamides ; Carcinoma, Neuroendocrine ; Cell Line, Tumor ; Cell Plasticity/drug effects ; Cell Plasticity/physiology ; Drug Resistance, Neoplasm ; Humans ; Male ; Mice ; Neoplastic Stem Cells/drug effects ; Neoplastic Stem Cells/metabolism ; Nitriles ; Phenylthiohydantoin ; Prostatic Neoplasms, Castration-Resistant/drug therapy ; Prostatic Neoplasms, Castration-Resistant/genetics ; Prostatic Neoplasms, Castration-Resistant/metabolism ; Receptors, Androgen/drug effects ; Receptors, Androgen/metabolism ; Signal Transduction ; Tumor Microenvironment/drug effects ; Tumor Microenvironment/physiology
    Chemical Substances Antineoplastic Agents ; Benzamides ; Nitriles ; Receptors, Androgen ; Phenylthiohydantoin (2010-15-3) ; enzalutamide (93T0T9GKNU)
    Language English
    Publishing date 2022-04-03
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2022.110595
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Stromal HIF2 Regulates Immune Suppression in the Pancreatic Cancer Microenvironment.

    Garcia Garcia, Carolina J / Huang, Yanqing / Fuentes, Natividad R / Turner, Madeleine C / Monberg, Maria E / Lin, Daniel / Nguyen, Nicholas D / Fujimoto, Tara N / Zhao, Jun / Lee, Jaewon J / Bernard, Vincent / Yu, Meifang / Delahoussaye, Abagail M / Jimenez Sacarello, Iancarlos / Caggiano, Emily G / Phan, Jae L / Deorukhkar, Amit / Molkentine, Jessica M / Saur, Dieter /
    Maitra, Anirban / Taniguchi, Cullen M

    Gastroenterology

    2022  Volume 162, Issue 7, Page(s) 2018–2031

    Abstract: Background & aims: Pancreatic ductal adenocarcinoma (PDAC) has a hypoxic, immunosuppressive stroma that contributes to its resistance to immune checkpoint blockade therapies. The hypoxia-inducible factors (HIFs) mediate the cellular response to hypoxia, ...

    Abstract Background & aims: Pancreatic ductal adenocarcinoma (PDAC) has a hypoxic, immunosuppressive stroma that contributes to its resistance to immune checkpoint blockade therapies. The hypoxia-inducible factors (HIFs) mediate the cellular response to hypoxia, but their role within the PDAC tumor microenvironment remains unknown.
    Methods: We used a dual recombinase mouse model to delete Hif1α or Hif2α in α-smooth muscle actin-expressing cancer-associated fibroblasts (CAFs) arising within spontaneous pancreatic tumors. The effects of CAF HIF2α expression on tumor progression and composition of the tumor microenvironment were evaluated by Kaplan-Meier analysis, reverse transcription quantitative real-time polymerase chain reaction, histology, immunostaining, and by both bulk and single-cell RNA sequencing. CAF-macrophage crosstalk was modeled ex vivo using conditioned media from CAFs after treatment with hypoxia and PT2399, an HIF2 inhibitor currently in clinical trials. Syngeneic flank and orthotopic PDAC models were used to assess whether HIF2 inhibition improves response to immune checkpoint blockade.
    Results: CAF-specific deletion of Hif2α, but not Hif1α, suppressed PDAC tumor progression and growth, and improved survival of mice by 50% (n = 21-23 mice/group, Log-rank P = .0009). Deletion of CAF-HIF2 modestly reduced tumor fibrosis and significantly decreased the intratumoral recruitment of immunosuppressive M2 macrophages and regulatory T cells. Treatment with the clinical HIF2 inhibitor PT2399 significantly reduced in vitro macrophage chemotaxis and M2 polarization, and improved tumor responses to immunotherapy in both syngeneic PDAC mouse models.
    Conclusions: Together, these data suggest that stromal HIF2 is an essential component of PDAC pathobiology and is a druggable therapeutic target that could relieve tumor microenvironment immunosuppression and enhance immune responses in this disease.
    MeSH term(s) Animals ; Cancer-Associated Fibroblasts/metabolism ; Carcinoma, Pancreatic Ductal/pathology ; Humans ; Hypoxia/metabolism ; Immune Checkpoint Inhibitors ; Immunosuppression Therapy ; Mice ; Pancreatic Neoplasms/pathology ; Tumor Microenvironment ; Pancreatic Neoplasms
    Chemical Substances Immune Checkpoint Inhibitors
    Language English
    Publishing date 2022-02-22
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80112-4
    ISSN 1528-0012 ; 0016-5085
    ISSN (online) 1528-0012
    ISSN 0016-5085
    DOI 10.1053/j.gastro.2022.02.024
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.MO 572: Show issues

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  4. Article ; Online: Nucleolin mediates the binding of cancer cells to L-selectin under conditions of lymphodynamic shear stress.

    Goldson, Tovë M / Turner, Kevin L / Huang, Yinan / Carlson, Grady E / Caggiano, Emily G / Oberhauser, Andres F / Fennewald, Susan M / Burdick, Monica M / Resto, Vicente A

    American journal of physiology. Cell physiology

    2019  Volume 318, Issue 1, Page(s) C83–C93

    Abstract: Head and neck squamous cell carcinoma (HNSCC) cells bind to lymphocytes via L-selectin in a shear-dependent manner. This interaction takes place exclusively under low-shear stress conditions, such as those found within the lymph node parenchyma. This ... ...

    Abstract Head and neck squamous cell carcinoma (HNSCC) cells bind to lymphocytes via L-selectin in a shear-dependent manner. This interaction takes place exclusively under low-shear stress conditions, such as those found within the lymph node parenchyma. This represents a novel functional role for L-selectin-selectin ligand interactions. Our previous work has characterized as-of-yet unidentified L-selectin ligands expressed by HNSCC cells that are specifically active under conditions of low shear stress consistent with lymph flow. Using an affinity purification approach, we now show that nucleolin expressed on the surface of HNSCC cells is an active ligand for L-selectin. Parallel plate chamber flow-based experiments and atomic force microscopy (AFM) experiments show that nucleolin is the main functional ligand under these low-force conditions. Furthermore, AFM shows a clear relationship between work of deadhesion and physiological loading rates. Our results reveal nucleolin as the first major ligand reported for L-selectin that operates under low-shear stress conditions.
    MeSH term(s) Cell Line, Tumor ; Gene Expression Regulation, Neoplastic ; Head and Neck Neoplasms/genetics ; Head and Neck Neoplasms/metabolism ; Head and Neck Neoplasms/pathology ; Humans ; L-Selectin/metabolism ; Ligands ; Lymphatic Metastasis ; Lymphatic Vessels/metabolism ; Lymphatic Vessels/pathology ; Phosphoproteins/genetics ; Phosphoproteins/metabolism ; Protein Binding ; RNA-Binding Proteins/genetics ; RNA-Binding Proteins/metabolism ; Signal Transduction ; Squamous Cell Carcinoma of Head and Neck/genetics ; Squamous Cell Carcinoma of Head and Neck/metabolism ; Squamous Cell Carcinoma of Head and Neck/pathology ; Stress, Mechanical ; Nucleolin
    Chemical Substances Ligands ; Phosphoproteins ; RNA-Binding Proteins ; SELL protein, human ; L-Selectin (126880-86-2)
    Language English
    Publishing date 2019-10-23
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 392098-7
    ISSN 1522-1563 ; 0363-6143
    ISSN (online) 1522-1563
    ISSN 0363-6143
    DOI 10.1152/ajpcell.00035.2019
    Database MEDical Literature Analysis and Retrieval System OnLINE

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