Inactivation of Myocardin and p16 during Malignant Transformation Contributes to a Differentiation Defect
Open Access
- 13 February 2007
- journal article
- Published by Elsevier BV in Cancer Cell
- Vol. 11 (2), 133-146
- https://doi.org/10.1016/j.ccr.2006.11.022
Abstract
No abstract availableKeywords
This publication has 32 references indexed in Scilit:
- hTERT-Immortalized Prostate Epithelial and Stromal-Derived Cells: an Authentic In vitro Model for Differentiation and CarcinogenesisCancer Research, 2006
- Loss of calponin h1 in renal angiomyolipoma correlates with aggressive clinical behaviorUrology, 2004
- Mechanisms of sarcoma developmentNature Reviews Cancer, 2003
- Myocardin Is a Critical Serum Response Factor Cofactor in the Transcriptional Program Regulating Smooth Muscle Cell DifferentiationMolecular and Cellular Biology, 2003
- Global Expression Profiling of Fibroblast Responses to Transforming Growth Factor-β1 Reveals the Induction of Inhibitor of Differentiation-1 and Provides Evidence of Smooth Muscle Cell Phenotypic SwitchingThe American Journal of Pathology, 2003
- Loss of p16Ink4a confers susceptibility to metastatic melanoma in miceNature, 2001
- Delineation of prognostic biomarkers in prostate cancerNature, 2001
- Possible Role of Calponin h1 as a Tumor Suppressor in Human Uterine LeiomyosarcomaJNCI Journal of the National Cancer Institute, 1999
- Correlation of Terminal Cell Cycle Arrest of Skeletal Muscle with Induction of p21 by MyoDScience, 1995
- Actin, its associated proteins and metastasisCell Motility, 1995