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  1. Article ; Online: A case of renomedullary interstitial cell tumor

    Kiyohito Yamamoto / Shigeru Kawabata / Yoshitaka Kurisu / Teruo Inamoto / Kazuhiro Yamamoto / Keigo Osuga

    Radiology Case Reports, Vol 18, Iss 12, Pp 4574-

    Radiologic-pathologic correlation

    2023  Volume 4579

    Abstract: Renomedullary interstitial cell tumor (RMICT), referred to as a medullary fibroma, is almost always asymptomatic and incidentally identified either at autopsy or upon resection of the kidney for other reasons. Although a few cases of RMICTs that are ... ...

    Abstract Renomedullary interstitial cell tumor (RMICT), referred to as a medullary fibroma, is almost always asymptomatic and incidentally identified either at autopsy or upon resection of the kidney for other reasons. Although a few cases of RMICTs that are large in size and clinically symptomatic have been reported, there are few reports of RMICTs contrasting imaging findings with pathological findings. In this report, we describe a relatively large RMICT case of 3 cm in size, focusing on the radiologic-pathologic correlation.
    Keywords Medullary fibroma ; Renal tumor ; Renomedullary interstitial cell tumor ; Medical physics. Medical radiology. Nuclear medicine ; R895-920
    Language English
    Publishing date 2023-12-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: Rapamycin Prevents the Development and Progression of Mutant Epidermal Growth Factor Receptor Lung Tumors with the Acquired Resistance Mutation T790M

    Shigeru Kawabata / José R. Mercado-Matos / M. Christine Hollander / Danielle Donahue / Willie Wilson III / Lucia Regales / Mohit Butaney / William Pao / Kwok-Kin Wong / Pasi A. Jänne / Phillip A. Dennis

    Cell Reports, Vol 7, Iss 6, Pp 1824-

    2014  Volume 1832

    Abstract: Lung cancer in never-smokers is an important disease often characterized by mutations in epidermal growth factor receptor (EGFR), yet risk reduction measures and effective chemopreventive strategies have not been established. We identify mammalian target ...

    Abstract Lung cancer in never-smokers is an important disease often characterized by mutations in epidermal growth factor receptor (EGFR), yet risk reduction measures and effective chemopreventive strategies have not been established. We identify mammalian target of rapamycin (mTOR) as potentially valuable target for EGFR mutant lung cancer. mTOR is activated in human lung cancers with EGFR mutations, and this increases with acquisition of T790M mutation. In a mouse model of EGFR mutant lung cancer, mTOR activation is an early event. As a single agent, the mTOR inhibitor rapamycin prevents tumor development, prolongs overall survival, and improves outcomes after treatment with an irreversible EGFR tyrosine kinase inhibitor (TKI). These studies support clinical testing of mTOR inhibitors in order to prevent the development and progression of EGFR mutant lung cancers.
    Keywords Biology (General) ; QH301-705.5
    Subject code 616
    Language English
    Publishing date 2014-06-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: A central role for Foxp3+ regulatory T cells in K-Ras-driven lung tumorigenesis.

    Courtney A Granville / Regan M Memmott / Andria Balogh / Jacopo Mariotti / Shigeru Kawabata / Wei Han / Jaclyn Lopiccolo / Jason Foley / David J Liewehr / Seth M Steinberg / Daniel H Fowler / M Christine Hollander / Phillip A Dennis

    PLoS ONE, Vol 4, Iss 3, p e

    2009  Volume 5061

    Abstract: K-Ras mutations are characteristic of human lung adenocarcinomas and occur almost exclusively in smokers. In preclinical models, K-Ras mutations are necessary for tobacco carcinogen-driven lung tumorigenesis and are sufficient to cause lung ... ...

    Abstract K-Ras mutations are characteristic of human lung adenocarcinomas and occur almost exclusively in smokers. In preclinical models, K-Ras mutations are necessary for tobacco carcinogen-driven lung tumorigenesis and are sufficient to cause lung adenocarcinomas in transgenic mice. Because these mutations confer resistance to commonly used cytotoxic chemotherapies and targeted agents, effective therapies that target K-Ras are needed. Inhibitors of mTOR such as rapamycin can prevent K-Ras-driven lung tumorigenesis and alter the proportion of cytotoxic and Foxp3+ regulatory T cells, suggesting that lung-associated T cells might be important for tumorigenesis.Lung tumorigenesis was studied in three murine models that depend on mutant K-Ras; a tobacco carcinogen-driven model, a syngeneic inoculation model, and a transgenic model. Splenic and lung-associated T cells were studied using flow cytometry and immunohistochemistry. Foxp3+ cells were depleted using rapamycin, an antibody, or genetic ablation.Exposure of A/J mice to a tobacco carcinogen tripled lung-associated Foxp3+ cells prior to tumor development. At clinically relevant concentrations, rapamycin prevented this induction and reduced lung tumors by 90%. In A/J mice inoculated with lung adenocarcinoma cells resistant to rapamycin, antibody-mediated depletion of Foxp3+ cells reduced lung tumorigenesis by 80%. Likewise, mutant K-Ras transgenic mice lacking Foxp3+ cells developed 75% fewer lung tumors than littermates with Foxp3+ cells.Foxp3+ regulatory T cells are required for K-Ras-mediated lung tumorigenesis in mice. These studies support clinical testing of rapamycin or other agents that target Treg in K-Ras driven human lung cancer.
    Keywords Medicine ; R ; Science ; Q
    Subject code 570 ; 610
    Language English
    Publishing date 2009-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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