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  1. AU="Lopez, Omar M"
  2. AU=Asfaw Abay
  3. AU="Santana, Ricardo Costa de"
  4. AU="Ortega, Johis"
  5. AU="Sogaolu, Moyosore"
  6. AU="Duchesne, Gabriela"
  7. AU="Sander, Klaus"
  8. AU="Wiegersma, Aline Marileen"
  9. AU=Mehta Yatin
  10. AU="Ki Hwan Kim"
  11. AU="Gulati, Rajiv"
  12. AU="Sullivan, Christopher"
  13. AU="Meier-Stephenson, Vanessa C"
  14. AU=Kim Joo Seop
  15. AU="Mortensen, Jennifer L"
  16. AU="Manthey, Helga D"
  17. AU="Baker, Susan"
  18. AU="Gunasegaram, James R"
  19. AU="Jung, Steffen"
  20. AU="Cairns, Anita"
  21. AU="Fox, Lindsay"

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  1. Artikel ; Online: Small-molecule targeted therapies induce dependence on DNA double-strand break repair in residual tumor cells.

    Ali, Moiez / Lu, Min / Ang, Hazel Xiaohui / Soderquist, Ryan S / Eyler, Christine E / Hutchinson, Haley M / Glass, Carolyn / Bassil, Christopher F / Lopez, Omar M / Kerr, D Lucas / Falcon, Christina J / Yu, Helena A / Hata, Aaron N / Blakely, Collin M / McCoach, Caroline E / Bivona, Trever G / Wood, Kris C

    Science translational medicine

    2022  Band 14, Heft 638, Seite(n) eabc7480

    Abstract: Residual cancer cells that survive drug treatments with targeted therapies act as a reservoir from which eventual resistant disease emerges. Although there is great interest in therapeutically targeting residual cells, efforts are hampered by our limited ...

    Abstract Residual cancer cells that survive drug treatments with targeted therapies act as a reservoir from which eventual resistant disease emerges. Although there is great interest in therapeutically targeting residual cells, efforts are hampered by our limited knowledge of the vulnerabilities existing in this cell state. Here, we report that diverse oncogene-targeted therapies, including inhibitors of epidermal growth factor receptor (EGFR), anaplastic lymphoma kinase (ALK), KRAS, and BRAF, induce DNA double-strand breaks and, consequently, ataxia-telangiectasia mutated (ATM)-dependent DNA repair in oncogene-matched residual tumor cells. This DNA damage response, observed in cell lines, mouse xenograft models, and human patients, is driven by a pathway involving the activation of caspases 3 and 7 and the downstream caspase-activated deoxyribonuclease (CAD). CAD is, in turn, activated through caspase-mediated degradation of its endogenous inhibitor, ICAD. In models of
    Mesh-Begriff(e) Animals ; Carcinoma, Non-Small-Cell Lung/drug therapy ; DNA ; DNA Repair ; Humans ; Lung Neoplasms/drug therapy ; Mice ; Neoplasm, Residual
    Chemische Substanzen DNA (9007-49-2)
    Sprache Englisch
    Erscheinungsdatum 2022-03-30
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2518854-9
    ISSN 1946-6242 ; 1946-6234
    ISSN (online) 1946-6242
    ISSN 1946-6234
    DOI 10.1126/scitranslmed.abc7480
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Generation and comparison of CRISPR-Cas9 and Cre-mediated genetically engineered mouse models of sarcoma.

    Huang, Jianguo / Chen, Mark / Whitley, Melodi Javid / Kuo, Hsuan-Cheng / Xu, Eric S / Walens, Andrea / Mowery, Yvonne M / Van Mater, David / Eward, William C / Cardona, Diana M / Luo, Lixia / Ma, Yan / Lopez, Omar M / Nelson, Christopher E / Robinson-Hamm, Jacqueline N / Reddy, Anupama / Dave, Sandeep S / Gersbach, Charles A / Dodd, Rebecca D /
    Kirsch, David G

    Nature communications

    2017  Band 8, Seite(n) 15999

    Abstract: Genetically engineered mouse models that employ site-specific recombinase technology are important tools for cancer research but can be costly and time-consuming. The CRISPR-Cas9 system has been adapted to generate autochthonous tumours in mice, but how ... ...

    Abstract Genetically engineered mouse models that employ site-specific recombinase technology are important tools for cancer research but can be costly and time-consuming. The CRISPR-Cas9 system has been adapted to generate autochthonous tumours in mice, but how these tumours compare to tumours generated by conventional recombinase technology remains to be fully explored. Here we use CRISPR-Cas9 to generate multiple subtypes of primary sarcomas efficiently in wild type and genetically engineered mice. These data demonstrate that CRISPR-Cas9 can be used to generate multiple subtypes of soft tissue sarcomas in mice. Primary sarcomas generated with CRISPR-Cas9 and Cre recombinase technology had similar histology, growth kinetics, copy number variation and mutational load as assessed by whole exome sequencing. These results show that sarcomas generated with CRISPR-Cas9 technology are similar to sarcomas generated with conventional modelling techniques and suggest that CRISPR-Cas9 can be used to more rapidly generate genotypically and phenotypically similar cancers.
    Mesh-Begriff(e) Animals ; CRISPR-Cas Systems ; Electroporation ; Gene Editing/methods ; Integrases ; Male ; Mice ; Mice, Nude ; Mutation ; NIH 3T3 Cells ; Neurilemmoma/genetics ; Neurilemmoma/pathology ; Sarcoma, Experimental/genetics ; Sarcoma, Experimental/pathology
    Chemische Substanzen Cre recombinase (EC 2.7.7.-) ; Integrases (EC 2.7.7.-)
    Sprache Englisch
    Erscheinungsdatum 2017-07-10
    Erscheinungsland England
    Dokumenttyp Comparative Study ; Evaluation Study ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/ncomms15999
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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