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  1. Article: The PDAC Extracellular Matrix: A Review of the ECM Protein Composition, Tumor Cell Interaction, and Therapeutic Strategies.

    Perez, Vincent M / Kearney, Joseph F / Yeh, Jen Jen

    Frontiers in oncology

    2021  Volume 11, Page(s) 751311

    Abstract: Pancreatic ductal adenocarcinoma (PDAC) is notorious for a dense fibrotic stroma that is interlaced with a collagen-based extracellular matrix (ECM) that plays an important role in tumor biology. Traditionally thought to only provide a physical barrier ... ...

    Abstract Pancreatic ductal adenocarcinoma (PDAC) is notorious for a dense fibrotic stroma that is interlaced with a collagen-based extracellular matrix (ECM) that plays an important role in tumor biology. Traditionally thought to only provide a physical barrier from host responses and systemic chemotherapy, new studies have demonstrated that the ECM maintains biomechanical and biochemical properties of the tumor microenvironment (TME) and restrains tumor growth. Recent studies have shown that the ECM augments tumor stiffness, interstitial fluid pressure, cell-to-cell junctions, and microvascularity using a mix of biomechanical and biochemical signals to influence tumor fate for better or worse. In addition, PDAC tumors have been shown to use ECM-derived peptide fragments as a nutrient source in nutrient-poor conditions. While collagens are the most abundant proteins found in the ECM, several studies have identified growth factors, integrins, glycoproteins, and proteoglycans in the ECM. This review focuses on the dichotomous nature of the PDAC ECM, the types of collagens and other proteins found in the ECM, and therapeutic strategies targeting the PDAC ECM.
    Language English
    Publishing date 2021-10-06
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2649216-7
    ISSN 2234-943X
    ISSN 2234-943X
    DOI 10.3389/fonc.2021.751311
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Shining a LIGHT on myeloid cell targeted immunotherapy.

    Shuptrine, Casey W / Perez, Vincent M / Selitsky, Sara R / Schreiber, Taylor H / Fromm, George

    European journal of cancer (Oxford, England : 1990)

    2023  Volume 187, Page(s) 147–160

    Abstract: Despite over a decade of clinical trials combining inhibition of emerging checkpoints with a PD-1/L1 inhibitor backbone, meaningful survival benefits have not been shown in PD-1/L1 inhibitor resistant or refractory solid tumours, particularly tumours ... ...

    Abstract Despite over a decade of clinical trials combining inhibition of emerging checkpoints with a PD-1/L1 inhibitor backbone, meaningful survival benefits have not been shown in PD-1/L1 inhibitor resistant or refractory solid tumours, particularly tumours dominated by a myelosuppressive microenvironment. Achieving durable anti-tumour immunity will therefore likely require combination of adaptive and innate immune stimulation, myeloid repolarisation, enhanced APC activation and antigen processing/presentation, lifting of the CD47/SIRPα (Cluster of Differentiation 47/signal regulatory protein alpha) 'do not eat me' signal, provision of an apoptotic 'pro-eat me' or 'find me' signal, and blockade of immune checkpoints. The importance of effectively targeting mLILRB2 and SIRPAyeloid cells to achieve improved response rates has recently been emphasised, given myeloid cells are abundant in the tumour microenvironment of most solid tumours. TNFSF14, or LIGHT, is a tumour necrosis superfamily ligand with a broad range of adaptive and innate immune activities, including (1) myeloid cell activation through Lymphotoxin Beta Receptor (LTβR), (2) T/NK (T cell and natural killer cell) induced anti-tumour immune activity through Herpes virus entry mediator (HVEM), (3) potentiation of proinflammatory cytokine/chemokine secretion through LTβR on tumour stromal cells, (4) direct induction of tumour cell apoptosis in vitro, and (5) the reorganisation of lymphatic tissue architecture, including within the tumour microenvironment (TME), by promoting high endothelial venule (HEV) formation and induction of tertiary lymphoid structures. LTBR (Lymphotoxin beta receptor) and HVEM rank highly amongst a range of costimulatory receptors in solid tumours, which raises interest in considering how LIGHT-mediated costimulation may be distinct from a growing list of immunotherapy targets which have failed to provide survival benefit as monotherapy or in combination with PD-1 inhibitors, particularly in the checkpoint acquired resistant setting.
    MeSH term(s) Humans ; Lymphotoxin beta Receptor ; Programmed Cell Death 1 Receptor ; Myeloid Cells ; Cytokines ; Neoplasms/drug therapy ; Immunotherapy ; Tumor Microenvironment
    Chemical Substances Lymphotoxin beta Receptor ; Programmed Cell Death 1 Receptor ; Cytokines
    Language English
    Publishing date 2023-04-05
    Publishing country England
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 82061-1
    ISSN 1879-0852 ; 0277-5379 ; 0959-8049 ; 0964-1947
    ISSN (online) 1879-0852
    ISSN 0277-5379 ; 0959-8049 ; 0964-1947
    DOI 10.1016/j.ejca.2023.03.040
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 456: Show issues Location:
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    Jg. 1995 - 2021: Lesesall (1.OG)
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  3. Article: Enhancing radiotherapy response via intratumoral injection of the TLR9 agonist CpG to stimulate CD8 T cells in an autochthonous mouse model of sarcoma.

    Su, Chang / Kent, Collin L / Pierpoint, Matthew / Floyd, Warren / Luo, Lixia / Wiliams, Nerissa T / Ma, Yan / Peng, Brian / Lazarides, Alexander L / Subramanian, Ajay / Himes, Jonathan E / Perez, Vincent M / Hernansaiz-Ballesteros, Rosa D / Roche, Kimberly E / Modliszewski, Jennifer L / Selitsky, Sara R / Mari Shinohara / Wisdom, Amy J / Moding, Everett J /
    Mowery, Yvonne M / Kirsch, David G

    bioRxiv : the preprint server for biology

    2024  

    Abstract: Radiation therapy is frequently used to treat cancers including soft tissue sarcomas. Prior studies established that the toll-like receptor 9 (TLR9) agonist cytosine-phosphate-guanine oligodeoxynucleotide (CpG) enhances the response to radiation therapy ( ...

    Abstract Radiation therapy is frequently used to treat cancers including soft tissue sarcomas. Prior studies established that the toll-like receptor 9 (TLR9) agonist cytosine-phosphate-guanine oligodeoxynucleotide (CpG) enhances the response to radiation therapy (RT) in transplanted tumors, but the mechanism(s) remain unclear. Here, we used CRISPR/Cas9 and the chemical carcinogen 3-methylcholanthrene (MCA) to generate autochthonous soft tissue sarcomas with high tumor mutation burden. Treatment with a single fraction of 20 Gy RT and two doses of CpG significantly enhanced tumor response, which was abrogated by genetic or immunodepletion of CD8+ T cells. To characterize the immune response to RT + CpG, we performed bulk RNA-seq, single-cell RNA-seq, and mass cytometry. Sarcomas treated with 20 Gy and CpG demonstrated increased CD8 T cells expressing markers associated with activation and proliferation, such as Granzyme B, Ki-67, and interferon-γ. CpG + RT also upregulated antigen presentation pathways on myeloid cells. Furthermore, in sarcomas treated with CpG + RT, TCR clonality analysis suggests an increase in clonal T-cell dominance. Collectively, these findings demonstrate that RT + CpG significantly delays tumor growth in a CD8 T cell-dependent manner. These results provide a strong rationale for clinical trials evaluating CpG or other TLR9 agonists with RT in patients with soft tissue sarcoma.
    Language English
    Publishing date 2024-01-04
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2024.01.03.573968
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: CSNK2B modulates IRF1 binding to functional DNA elements and promotes basal and agonist-induced antiviral signaling.

    Matsumoto, Moe / Modliszewski, Jennifer L / Shinozaki, Kotomi / Maezawa, Reona / Perez, Vincent M / Ishikawa, Yuki / Suzuki, Ryosuke / McKnight, Kevin L / Masaki, Takahiro / Hirai-Yuki, Asuka / Kohara, Michinori / Lemon, Stanley M / Selitsky, Sara R / Yamane, Daisuke

    Nucleic acids research

    2023  Volume 51, Issue 9, Page(s) 4451–4466

    Abstract: Interferon regulatory factor 1 (IRF1) is a critical component of cell-intrinsic innate immunity that regulates both constitutive and induced antiviral defenses. Due to its short half-life, IRF1 function is generally considered to be regulated by its ... ...

    Abstract Interferon regulatory factor 1 (IRF1) is a critical component of cell-intrinsic innate immunity that regulates both constitutive and induced antiviral defenses. Due to its short half-life, IRF1 function is generally considered to be regulated by its synthesis. However, how IRF1 activity is controlled post-translationally has remained poorly characterized. Here, we employed a proteomics approach to identify proteins interacting with IRF1, and found that CSNK2B, a regulatory subunit of casein kinase 2, interacts directly with IRF1 and constitutively modulates its transcriptional activity. Genome-wide CUT&RUN analysis of IRF1 binding loci revealed that CSNK2B acts generally to enhance the binding of IRF1 to chromatin, thereby enhancing transcription of key antiviral genes, such as PLAAT4 (also known as RARRES3/RIG1/TIG3). On the other hand, depleting CSNK2B triggered abnormal accumulation of IRF1 at AFAP1 loci, thereby down-regulating transcription of AFAP1, revealing contrary effects of CSNK2B on IRF1 binding at different loci. AFAP1 encodes an actin crosslinking factor that mediates Src activation. Importantly, CSNK2B was also found to mediate phosphorylation-dependent activation of AFAP1-Src signaling and exert suppressive effects against flaviviruses, including dengue virus. These findings reveal a previously unappreciated mode of IRF1 regulation and identify important effector genes mediating multiple cellular functions governed by CSNK2B and IRF1.
    MeSH term(s) Chromatin ; DNA/genetics ; Interferon Regulatory Factor-1/genetics ; Signal Transduction/genetics ; Humans ; Casein Kinase II/genetics ; Immunity, Innate ; Virus Diseases/genetics ; Virus Diseases/immunology
    Chemical Substances Chromatin ; DNA (9007-49-2) ; Interferon Regulatory Factor-1 ; Casein Kinase II (EC 2.7.11.1) ; IRF1 protein, human
    Language English
    Publishing date 2023-04-25
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 186809-3
    ISSN 1362-4962 ; 1362-4954 ; 0301-5610 ; 0305-1048
    ISSN (online) 1362-4962 ; 1362-4954
    ISSN 0301-5610 ; 0305-1048
    DOI 10.1093/nar/gkad298
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1067: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
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  5. Article ; Online: Deletion of fatty acid transport protein 2 (FATP2) in the mouse liver changes the metabolic landscape by increasing the expression of PPARα-regulated genes.

    Perez, Vincent M / Gabell, Jeffrey / Behrens, Mark / Wase, Nishikant / DiRusso, Concetta C / Black, Paul N

    The Journal of biological chemistry

    2020  Volume 295, Issue 17, Page(s) 5737–5750

    Abstract: Fatty acid transport protein 2 (FATP2) is highly expressed in the liver, small intestine, and kidney, where it functions in both the transport of exogenous long-chain fatty acids and the activation of very-long-chain fatty acids. Here, using a murine ... ...

    Abstract Fatty acid transport protein 2 (FATP2) is highly expressed in the liver, small intestine, and kidney, where it functions in both the transport of exogenous long-chain fatty acids and the activation of very-long-chain fatty acids. Here, using a murine model, we investigated the phenotypic impacts of deleting FATP2, followed by a transcriptomic analysis using unbiased RNA-Seq to identify concomitant changes in the liver transcriptome. WT and FATP2-null (
    MeSH term(s) Animals ; Coenzyme A Ligases/genetics ; Coenzyme A Ligases/metabolism ; Female ; Gene Deletion ; Gene Expression Regulation ; Lipid Metabolism ; Liver/metabolism ; Male ; Metabolome ; Mice ; Mice, Inbred C57BL ; PPAR alpha/genetics ; PPAR alpha/metabolism ; Transcriptome
    Chemical Substances PPAR alpha ; Coenzyme A Ligases (EC 6.2.1.-) ; FATP2 protein, mouse (EC 6.2.1.-)
    Language English
    Publishing date 2020-03-18
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1074/jbc.RA120.012730
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.108: Show issues Location:
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