D W Felsher
Affiliation: University of California
- Transient excess of MYC activity can elicit genomic instability and tumorigenesisD 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...
- Reversible tumorigenesis by MYC in hematopoietic lineagesD 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...
- Overexpression of MYC causes p53-dependent G2 arrest of normal fibroblastsD 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...
- c-Myc is a critical target for c/EBPalpha in granulopoiesisL 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...