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Research Article

Signature-Based Small Molecule Screening Identifies Cytosine Arabinoside as an EWS/FLI Modulator in Ewing Sarcoma

  • Kimberly Stegmaier,

    Affiliations: Department of Pediatric Oncology, Dana-Farber Cancer Institute and Children's Hospital Boston, Harvard Medical School, Boston, Massachusetts, United States of America, The Broad Institute of Harvard University and Massachusetts Institute of Technology, Cambridge, Massachusetts, United States of America

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  • Jenny S Wong,

    Affiliations: Department of Pediatric Oncology, Dana-Farber Cancer Institute and Children's Hospital Boston, Harvard Medical School, Boston, Massachusetts, United States of America, Howard Hughes Medical Institute, Harvard Medical School, Boston, Massachusetts, United States of America

    X
  • Kenneth N Ross,

    Affiliation: The Broad Institute of Harvard University and Massachusetts Institute of Technology, Cambridge, Massachusetts, United States of America

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  • Kwan T Chow,

    Affiliation: Department of Pediatric Oncology, Dana-Farber Cancer Institute and Children's Hospital Boston, Harvard Medical School, Boston, Massachusetts, United States of America

    X
  • David Peck,

    Affiliation: The Broad Institute of Harvard University and Massachusetts Institute of Technology, Cambridge, Massachusetts, United States of America

    X
  • Renee D Wright,

    Affiliation: Department of Pediatric Oncology, Dana-Farber Cancer Institute and Children's Hospital Boston, Harvard Medical School, Boston, Massachusetts, United States of America

    X
  • Stephen L Lessnick,

    Affiliation: The Center for Children, Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah, United States of America

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  • Andrew L Kung,

    Affiliation: Department of Pediatric Oncology, Dana-Farber Cancer Institute and Children's Hospital Boston, Harvard Medical School, Boston, Massachusetts, United States of America

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  • Todd R Golub mail

    To whom correspondence should be addressed. E-mail: golub@broad.mit.edu

    Affiliations: Department of Pediatric Oncology, Dana-Farber Cancer Institute and Children's Hospital Boston, Harvard Medical School, Boston, Massachusetts, United States of America, The Broad Institute of Harvard University and Massachusetts Institute of Technology, Cambridge, Massachusetts, United States of America, Howard Hughes Medical Institute, Harvard Medical School, Boston, Massachusetts, United States of America

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  • Published: April 10, 2007
  • DOI: 10.1371/journal.pmed.0040122

Reader Comments (1)

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Data not in agreement with authors' interpretation

Posted by plosmedicine on 31 Mar 2009 at 00:10 GMT

Author: Idriss Bennani-Baiti
Position: Staff Scientist
Institution: Children's Cancer Research Institute
E-mail: idriss.bennani@ccri.at
Submitted Date: June 15, 2007
Published Date: June 18, 2007
This comment was originally posted as a “Reader Response” on the publication date indicated above. All Reader Responses are now available as comments.

My comment concerns Supplementary Fig.1. In the AraC-treated cells, only four out of 12 genes (FHL2, SSX2, SSX3, and GLI) cluster to some extent with the Ews-Fli1 ShRNA-treated subset. The remaining 8 genes cluster with the untreated cells.

I am not sure how these data substantiate the authors claim, namely that "ARA-C Induces an EWS/FLI Off Signature in A673 Ewing Sarcoma Cells".

It might help to provide Affy. data from treated and non-treated cells of a larger pool of genes. The significance of data might become both meaningful and obvious to the reader.

Kindest regards,

No competing interests declared.