D W Felsher

Summary

Affiliation: University of California
Country: USA

Publications

  1. pmc Transient excess of MYC activity can elicit genomic instability and tumorigenesis
    D W Felsher
    Division of Hematology Oncology, Department of Medicine, University of California, San Francisco 94143 1270, USA
    Proc Natl Acad Sci U S A 96:3940-4. 1999
  2. ncbi Reversible tumorigenesis by MYC in hematopoietic lineages
    D W Felsher
    Department of Medicine, G W Hooper Foundation, San Francisco, California, USA
    Mol Cell 4:199-207. 1999
  3. pmc Overexpression of MYC causes p53-dependent G2 arrest of normal fibroblasts
    D W Felsher
    Division of Oncology, Departments of Medicine and Pathology, Stanford University, Stanford, CA 94305 5115, USA
    Proc Natl Acad Sci U S A 97:10544-8. 2000
  4. pmc c-Myc is a critical target for c/EBPalpha in granulopoiesis
    L M Johansen
    Harvard Institutes of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA
    Mol Cell Biol 21:3789-806. 2001

Collaborators

  • L M Johansen
  • K Sasaki
  • D G Tenen
  • T A Lodie
  • T R Golub
  • A Iwama

Detail Information

Publications4

  1. pmc Transient excess of MYC activity can elicit genomic instability and tumorigenesis
    D W Felsher
    Division of Hematology Oncology, Department of Medicine, University of California, San Francisco 94143 1270, USA
    Proc Natl Acad Sci U S A 96:3940-4. 1999
    ..We suggest that the accelerated passage through G1 was mutagenic but that the effect of MYC permitted a checkpoint response only after G2 had been reached. Thus, MYC may contribute to tumorigenesis through a dominant mutator effect...
  2. ncbi Reversible tumorigenesis by MYC in hematopoietic lineages
    D W Felsher
    Department of Medicine, G W Hooper Foundation, San Francisco, California, USA
    Mol Cell 4:199-207. 1999
    ..We conclude that even though tumorigenesis is a multistep process, remediation of a single genetic lesion may be sufficient to reverse malignancy...
  3. pmc Overexpression of MYC causes p53-dependent G2 arrest of normal fibroblasts
    D W Felsher
    Division of Oncology, Departments of Medicine and Pathology, Stanford University, Stanford, CA 94305 5115, USA
    Proc Natl Acad Sci U S A 97:10544-8. 2000
    ..The loss of p53 function seems to be one mechanism by which this relaxation commonly occurs. These findings dramatize how multiple genetic events can collaborate to produce neoplastic cells...
  4. pmc c-Myc is a critical target for c/EBPalpha in granulopoiesis
    L M Johansen
    Harvard Institutes of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA
    Mol Cell Biol 21:3789-806. 2001
    ..This is the first report to demonstrate that C/EBPalpha directly affects the level of c-Myc expression and, thus, the decision of myeloid blasts to enter into the granulocytic differentiation pathway...