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  1. Book: Receptor tyrosine kinases

    Yarden, Yosef / Wheeler, Deric L.

    family and subfamilies

    2015  

    Author's details Deric L. Wheeler ; Yosef Yarden ed
    Keywords Rezeptor-Tyrosinkinasen
    Subject RTK ; RYK ; EC 2.7.10.1 ; Receptor Protein-Tyrosine Kinases ; Protein-Tyrosine Kinase Receptor ; PTK Receptors ; Receptor Protein-Tyrosine Kinase ; Tyrosine Kinase Receptors
    Language English
    Size XVII, 878 S. : Ill., graph. Darst.
    Publisher Humana Press
    Publishing place New York u.a.
    Publishing country United States
    Document type Book
    HBZ-ID HT018733046
    ISBN 978-3-319-11887-1 ; 9783319118888 ; 3-319-11887-0 ; 3319118889
    Database Catalogue ZB MED Medicine, Health

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  2. Book: Receptor tyrosine kinases

    Yarden, Yosef / Wheeler, Deric L.

    structure, functions and role in human disease

    2015  

    Author's details Deric L. Wheeler ; Yosef Yarden ed
    Keywords Rezeptor-Tyrosinkinasen
    Subject RTK ; RYK ; EC 2.7.10.1 ; Receptor Protein-Tyrosine Kinases ; Protein-Tyrosine Kinase Receptor ; PTK Receptors ; Receptor Protein-Tyrosine Kinase ; Tyrosine Kinase Receptors
    Language English
    Size XVII, 440 S. : Ill., graph. Darst.
    Publisher Humana Press
    Publishing place New York u.a.
    Publishing country United States
    Document type Book
    Note Literaturangaben
    HBZ-ID HT018653105
    ISBN 978-1-4939-2052-5 ; 9781493920532 ; 1-4939-2052-9 ; 1493920537
    Database Catalogue ZB MED Medicine, Health

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  3. Article: Immune Escape Strategies in Head and Neck Cancer: Evade, Resist, Inhibit, Recruit.

    Kostecki, Kourtney L / Iida, Mari / Crossman, Bridget E / Salgia, Ravi / Harari, Paul M / Bruce, Justine Y / Wheeler, Deric L

    Cancers

    2024  Volume 16, Issue 2

    Abstract: Head and neck cancers (HNCs) arise from the mucosal lining of the aerodigestive tract and are often associated with alcohol use, tobacco use, and/or human papillomavirus (HPV) infection. Over 600,000 new cases of HNC are diagnosed each year, making it ... ...

    Abstract Head and neck cancers (HNCs) arise from the mucosal lining of the aerodigestive tract and are often associated with alcohol use, tobacco use, and/or human papillomavirus (HPV) infection. Over 600,000 new cases of HNC are diagnosed each year, making it the sixth most common cancer worldwide. Historically, treatments have included surgery, radiation, and chemotherapy, and while these treatments are still the backbone of current therapy, several immunotherapies have recently been approved by the Food and Drug Administration (FDA) for use in HNC. The role of the immune system in tumorigenesis and cancer progression has been explored since the early 20th century, eventually coalescing into the current three-phase model of cancer immunoediting. During each of the three phases-elimination, equilibrium, and escape-cancer cells develop and utilize multiple strategies to either reach or remain in the final phase, escape, at which point the tumor is able to grow and metastasize with little to no detrimental interference from the immune system. In this review, we summarize the many strategies used by HNC to escape the immune system, which include ways to evade immune detection, resist immune cell attacks, inhibit immune cell functions, and recruit pro-tumor immune cells.
    Language English
    Publishing date 2024-01-11
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers16020312
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Radiation Sensitivity: The Rise of Predictive Patient-Derived Cancer Models.

    Berube, Liliana L / Nickel, Kwang-Ok P / Iida, Mari / Ramisetty, Sravani / Kulkarni, Prakash / Salgia, Ravi / Wheeler, Deric L / Kimple, Randall J

    Seminars in radiation oncology

    2023  Volume 33, Issue 3, Page(s) 279–286

    Abstract: Patient-derived cancer models have been used for decades to improve our understanding of cancer and test anticancer treatments. Advances in radiation delivery have made these models more attractive for studying radiation sensitizers and understanding an ... ...

    Abstract Patient-derived cancer models have been used for decades to improve our understanding of cancer and test anticancer treatments. Advances in radiation delivery have made these models more attractive for studying radiation sensitizers and understanding an individual patient's radiation sensitivity. Advances in the use of patient-derived cancer models lead to a more clinically relevant outcome, although many questions remain regarding the optimal use of patient-derived xenografts and patient-derived spheroid cultures. The use of patient-derived cancer models as personalized predictive avatars through mouse and zebrafish models is discussed, and the advantages and disadvantages of patient-derived spheroids are reviewed. In addition, the use of large repositories of patient-derived models to develop predictive algorithms to guide treatment selection is discussed. Finally, we review methods for establishing patient-derived models and identify key factors that influence their use as both avatars and models of cancer biology.
    MeSH term(s) Humans ; Mice ; Animals ; Zebrafish ; Neoplasms/radiotherapy ; Disease Models, Animal ; Radiation Tolerance
    Language English
    Publishing date 2023-06-19
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1146999-7
    ISSN 1532-9461 ; 1053-4296
    ISSN (online) 1532-9461
    ISSN 1053-4296
    DOI 10.1016/j.semradonc.2023.03.005
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Active recruitment of anti-PD-1-conjugated platelets through tumor-selective thrombosis for enhanced anticancer immunotherapy.

    Wang, Yixin / Li, Wen / Li, Zhaoting / Mo, Fanyi / Chen, Yu / Iida, Mari / Wheeler, Deric L / Hu, Quanyin

    Science advances

    2023  Volume 9, Issue 13, Page(s) eadf6854

    Abstract: Immune checkpoint inhibitors (ICIs) can reinvigorate T cells to eradicate tumor cells, showing great potential in combating various types of tumors. We propose a delivery strategy to enhance tumor-selective ICI accumulation, which leverages the ... ...

    Abstract Immune checkpoint inhibitors (ICIs) can reinvigorate T cells to eradicate tumor cells, showing great potential in combating various types of tumors. We propose a delivery strategy to enhance tumor-selective ICI accumulation, which leverages the responsiveness of platelets and platelet-derivatives to coagulation cascade signals. A fused protein tTF-RGD targets tumor angiogenic blood vessel endothelial cells and initiates the coagulation locoregionally at the tumor site, forming a "cellular hive" to recruit anti-PD-1 antibody (aPD-1)-conjugated platelets to the tumor site and subsequently activating platelets to release aPD-1 antibody to reactivate T cells for improved immunotherapy. Moreover, on a patient-derived xenograft breast cancer model, the platelet membrane-coated nanoparticles can also respond to the coagulation signals initiated by tTF-RGD, thus enhancing the accumulation and antitumor efficacy of the loaded chemotherapeutics. Our study illustrates a versatile platform technology to enhance the local accumulation of ICIs and chemodrugs by taking advantage of the responsiveness of platelets and platelet derivatives to thrombosis.
    MeSH term(s) Animals ; Humans ; Disease Models, Animal ; Endothelial Cells ; Immunotherapy ; Neoplasms/drug therapy ; Oligopeptides ; Thrombosis/drug therapy ; Thrombosis/etiology ; Programmed Cell Death 1 Receptor/immunology
    Chemical Substances Oligopeptides ; Programmed Cell Death 1 Receptor
    Language English
    Publishing date 2023-03-29
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2810933-8
    ISSN 2375-2548 ; 2375-2548
    ISSN (online) 2375-2548
    ISSN 2375-2548
    DOI 10.1126/sciadv.adf6854
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Book: Receptor tyrosine kinases

    Wheeler, Deric L / Yarden, Y

    2015  

    Title variant Structure, functions and role in human disease
    Author's details Deric L. Wheeler, Yosef Yarden, editors
    MeSH term(s) Receptor Protein-Tyrosine Kinases
    Language English
    Size xvii, 440 pages :, illustrations, portraits
    Document type Book
    ISBN 9781493920525 ; 9781493920532 ; 1493920529 ; 1493920537
    Database Catalogue of the US National Library of Medicine (NLM)

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  7. Book: Receptor tyrosine kinases

    Wheeler, Deric L / Yarden, Y

    2015  

    Title variant Family and subfamilies
    Author's details Deric L. Wheeler, Yosef Yarden, editors
    MeSH term(s) Receptor Protein-Tyrosine Kinases
    Language English
    Size xvii, 878 pages :, illustrations (chiefly color)
    Document type Book
    ISBN 9783319118871 ; 3319118870 ; 9783319118888 ; 3319118889
    Database Catalogue of the US National Library of Medicine (NLM)

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  8. Article ; Online: Feedback regulation of biological networks: Examples relevant to signalling pathways and resistance to pharmacological interceptors.

    Yarden, Yosef / Wheeler, Deric L

    Seminars in cell & developmental biology

    2016  Volume 50, Page(s) 83–84

    MeSH term(s) Animals ; Antineoplastic Agents/pharmacology ; Dual Specificity Phosphatase 1/metabolism ; Feedback, Physiological ; Humans ; Pharmaceutical Preparations/metabolism ; Protein Kinases/metabolism ; Receptors, G-Protein-Coupled/metabolism ; Signal Transduction
    Chemical Substances Antineoplastic Agents ; Pharmaceutical Preparations ; Receptors, G-Protein-Coupled ; Protein Kinases (EC 2.7.-) ; Dual Specificity Phosphatase 1 (EC 3.1.3.48)
    Language English
    Publishing date 2016-02
    Publishing country England
    Document type Editorial ; Introductory Journal Article
    ZDB-ID 1312473-0
    ISSN 1096-3634 ; 1084-9521
    ISSN (online) 1096-3634
    ISSN 1084-9521
    DOI 10.1016/j.semcdb.2016.02.016
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Dual Axl/MerTK inhibitor INCB081776 creates a proinflammatory tumor immune microenvironment and enhances anti-PDL1 efficacy in head and neck cancer.

    Kostecki, Kourtney L / Iida, Mari / Wiley, Anne L / Kimani, Stanley / Mehall, Bridget / Tetreault, Kaitlin / Alexandridis, Roxana / Yu, Menggang / Hong, Seungpyo / Salgia, Ravi / Bruce, Justine Y / Birge, Raymond B / Harari, Paul M / Wheeler, Deric L

    Head & neck

    2023  Volume 45, Issue 5, Page(s) 1255–1271

    Abstract: Background: The tyrosine kinase receptors Axl and MerTK are highly overexpressed in head and neck cancer (HNC) cells, where they are critical drivers of survival, proliferation, metastasis, and therapeutic resistance.: Methods: We investigated the ... ...

    Abstract Background: The tyrosine kinase receptors Axl and MerTK are highly overexpressed in head and neck cancer (HNC) cells, where they are critical drivers of survival, proliferation, metastasis, and therapeutic resistance.
    Methods: We investigated the role of Axl and MerTK in creating an immunologically "cold" tumor immune microenvironment (TIME) by targeting both receptors simultaneously with a small molecule inhibitor of Axl and MerTK (INCB081776). Effects of INCB081776 and/or anti-PDL1 on mouse oral cancer (MOC) cell growth and on the TIME were evaluated.
    Results: Targeting Axl and MerTK can reduce M
    Conclusions: This data indicates that simultaneous targeting of Axl and MerTK with INCB081776, either alone or in combination with anti-PDL1, slows tumor growth and creates a proinflammatory TIME in mouse models of HNC.
    MeSH term(s) Animals ; Mice ; c-Mer Tyrosine Kinase ; Cell Line, Tumor ; Head and Neck Neoplasms ; Protein Kinase Inhibitors/pharmacology ; Proto-Oncogene Proteins ; Tumor Microenvironment
    Chemical Substances atezolizumab (52CMI0WC3Y) ; c-Mer Tyrosine Kinase (EC 2.7.10.1) ; Mertk protein, mouse (EC 2.7.10.1) ; Protein Kinase Inhibitors ; Proto-Oncogene Proteins ; AXL receptor tyrosine kinase, mouse
    Language English
    Publishing date 2023-03-20
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 645165-2
    ISSN 1097-0347 ; 0148-6403 ; 1043-3074
    ISSN (online) 1097-0347
    ISSN 0148-6403 ; 1043-3074
    DOI 10.1002/hed.27340
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Targeting HER3-dependent activation of nuclear AKT improves radiotherapy of non-small cell lung cancer.

    Toulany, Mahmoud / Iida, Mari / Lettau, Konstanze / Coan, John P / Rebholz, Simone / Khozooei, Shayan / Harari, Paul M / Wheeler, Deric L

    Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology

    2022  Volume 174, Page(s) 92–100

    Abstract: Background: AKT1 must be present and activated in the nucleus immediately after irradiation to stimulate AKT1-dependent double-strand breaks (DSB) repair through the fast non-homologous end-joining (NHEJ) repair process. We investigated the subcellular ... ...

    Abstract Background: AKT1 must be present and activated in the nucleus immediately after irradiation to stimulate AKT1-dependent double-strand breaks (DSB) repair through the fast non-homologous end-joining (NHEJ) repair process. We investigated the subcellular distribution of AKT1 and the role of HER family receptor members on the phosphorylation of nuclear AKT and radiation response.
    Materials and methods: Using genetic approaches and pharmacological inhibitors, we investigated the subcellular distribution of AKT1 and the role of HER family receptor members on the activation of nuclear AKT in non-small cell lung cancer (NSCLC) cells in vitro. ɤH2AX foci assay was applied to investigate the role of AKT activating signaling pathway on DSB repair. A mouse tumor xenograft model was used to study the impact of discovered signaling pathway activating nuclear AKT on the radiation response of tumors in vivo.
    Results: Our data suggests that neither ionizing radiation (IR) nor stimulation with HER family receptor ligands induced rapid nuclear translocation of endogenous AKT1. GFP-tagged exogenous AKT1 translocated to the nucleus under un-irradiated conditions and IR did not stimulate this translocation. Nuclear translocation of GFP-AKT1 was impaired by the AKT inhibitor MK2206 as shown by its accumulation in the cytoplasmic fraction. IR-induced phosphorylation of nuclear AKT was primarily dependent on HER3 expression and tyrosine kinase activation of epidermal growth factor receptor. In line with the role of AKT1 in DSB repair, the HER3 neutralizing antibody patritumab as well as HER3-siRNA diminished DSB repair in vitro. Combination of patritumab with radiotherapy improved the effect of radiotherapy on tumor growth delay in a xenograft model.
    Conclusion: IR-induced activation of nuclear AKT occurs inside the nucleus that is mainly dependent on HER3 expression in NSCLC. These findings suggest that targeting HER3 in combination with radiotherapy may provide a logical treatment option for investigation in selected NSCLC patients.
    MeSH term(s) Animals ; Antibodies, Neutralizing/genetics ; Carcinoma, Non-Small-Cell Lung/genetics ; Cell Line, Tumor ; DNA Breaks, Double-Stranded ; DNA Repair ; ErbB Receptors/genetics ; Humans ; Lung Neoplasms/metabolism ; Lung Neoplasms/radiotherapy ; Mice ; Proto-Oncogene Proteins c-akt/genetics ; Proto-Oncogene Proteins c-akt/metabolism ; RNA, Small Interfering
    Chemical Substances Antibodies, Neutralizing ; RNA, Small Interfering ; ErbB Receptors (EC 2.7.10.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
    Language English
    Publishing date 2022-07-15
    Publishing country Ireland
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 605646-5
    ISSN 1879-0887 ; 0167-8140
    ISSN (online) 1879-0887
    ISSN 0167-8140
    DOI 10.1016/j.radonc.2022.07.008
    Database MEDical Literature Analysis and Retrieval System OnLINE

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