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  1. Article ; Online: Development of the aganglionic colon following surgical rescue in a cell therapy model of Hirschsprung disease in rat

    John B. Furness / Enie Lei / Billie Hunne / Cameron D. Adams / Alan J. Burns / Jill Wykosky / Therese E. Fazio Coles / Linda J. Fothergill / Juan C. Molero / Ruslan V. Pustovit / Lincon A. Stamp

    Disease Models & Mechanisms, Vol 16, Iss

    2023  Volume 6

    Keywords hirschsprung disease ; stem cell therapy ; colon ; intestinal bypass ; enteric neurons ; enteric nervous system ; Medicine ; R ; Pathology ; RB1-214
    Language English
    Publishing date 2023-06-01T00:00:00Z
    Publisher The Company of Biologists
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article: Targeted Therapy Resistance Mediated by Dynamic Regulation of Extrachromosomal Mutant EGFR DNA

    Nathanson, David A / Andres Paucar / Ascia Eskin / Beatrice Gini / C. David James / Frank B. Furnari / German Gomez / Harley I. Kornblum / Huijun Yang / Jack Mottahedeh / James R. Heath / Jill Wykosky / Jun Wang / Kenta Masui / Kiwook Hwang / Koppany Visnyei / Minori Ohashi / P. Nagesh Rao / Paul S. Mischel /
    Rachel Reed / Shaojun Zhu / Stanley F. Nelson / Timothy F. Cloughesy / Tomoyuki Koga / Webster K. Cavenee

    Science. 2014 Jan. 3, v. 343, no. 6166

    2014  

    Abstract: Playing Hide and Seek Targeted cancer therapies have shown promising results in patients, but few of these drugs provide long-term benefits because tumor cells rapidly develop drug resistance. Nathanson et al. (p. 72, published online 5 December) show ... ...

    Abstract Playing Hide and Seek Targeted cancer therapies have shown promising results in patients, but few of these drugs provide long-term benefits because tumor cells rapidly develop drug resistance. Nathanson et al. (p. 72, published online 5 December) show that glioblastoma cells can become resistant to erlotinib, an epidermal growth factor receptor (EGFR)–targeted drug, by eliminating extrachromosomal copies of the mutant EGFR gene. After a period of drug withdrawal, the mutant EGFR gene reappears on extrachromosomal DNA and the tumor cells become resensitized. The discovery that cancer cells can evade drug therapy by this “hide and seek” mechanism may help to optimize the dosing schedule of erlotinib in glioblastoma patients.
    Keywords DNA ; drug resistance ; drug therapy ; drugs ; epidermal growth factor receptors ; genes ; mutants ; neoplasm cells ; neoplasms ; patients
    Language English
    Dates of publication 2014-0103
    Size p. 72-76.
    Publishing place American Association for the Advancement of Science
    Document type Article
    ZDB-ID 128410-1
    ISSN 1095-9203 ; 0036-8075
    ISSN (online) 1095-9203
    ISSN 0036-8075
    DOI 10.1126/science.1241328
    Database NAL-Catalogue (AGRICOLA)

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  3. Article ; Online: Targeting EGFR induced oxidative stress by PARP1 inhibition in glioblastoma therapy.

    Masayuki Nitta / David Kozono / Richard Kennedy / Jayne Stommel / Kimberly Ng / Pascal O Zinn / Deepa Kushwaha / Santosh Kesari / Maria-del-Mar Inda / Jill Wykosky / Frank Furnari / Katherine A Hoadley / Lynda Chin / Ronald A DePinho / Webster K Cavenee / Alan D'Andrea / Clark C Chen

    PLoS ONE, Vol 5, Iss 5, p e

    2010  Volume 10767

    Abstract: Despite the critical role of Epidermal Growth Factor Receptor (EGFR) in glioblastoma pathogenesis, EGFR targeted therapies have achieved limited clinical efficacy. Here we propose an alternate therapeutic strategy based on the conceptual framework of non- ...

    Abstract Despite the critical role of Epidermal Growth Factor Receptor (EGFR) in glioblastoma pathogenesis, EGFR targeted therapies have achieved limited clinical efficacy. Here we propose an alternate therapeutic strategy based on the conceptual framework of non-oncogene addiction. A directed RNAi screen revealed that glioblastoma cells over-expressing EGFRvIII, an oncogenic variant of EGFR, become hyper-dependent on a variety of DNA repair genes. Among these, there was an enrichment of Base Excision Repair (BER) genes required for the repair of Reactive Oxygen Species (ROS)-induced DNA damage, including poly-ADP ribose polymerase 1 (PARP1). Subsequent studies revealed that EGFRvIII over-expression in glioblastoma cells caused increased levels of ROS, DNA strand break accumulation, and genome instability. In a panel of primary glioblastoma lines, sensitivity to PARP1 inhibition correlated with the levels of EGFR activation and oxidative stress. Gene expression analysis indicated that reduced expression of BER genes in glioblastomas with high EGFR expression correlated with improved patient survival. These observations suggest that oxidative stress secondary to EGFR hyper-activation necessitates increased cellular reliance on PARP1 mediated BER, and offer critical insights into clinical trial design.
    Keywords Medicine ; R ; Science ; Q
    Subject code 616
    Language English
    Publishing date 2010-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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