TGF-β Receptor Inactivation and Mutant Kras Induce Intestinal Neoplasms in Mice via a β-Catenin-Independent Pathway
Open Access
- 31 May 2009
- journal article
- research article
- Published by Elsevier BV in Gastroenterology
- Vol. 136 (5), 1680-1688.e7
- https://doi.org/10.1053/j.gastro.2009.01.066
Abstract
No abstract availableFunding Information
- National Cancer Institute (RO1CA115513)
- U.S. Department of Veterans Affairs (5 P30 CA015704)
This publication has 37 references indexed in Scilit:
- Differential effects of oncogenic K-Ras and N-Ras on proliferation, differentiation and tumor progression in the colonNature Genetics, 2008
- Phenotypically Concordant and Discordant Monozygotic Twins Display Different DNA Copy-Number-Variation ProfilesAmerican Journal of Human Genetics, 2008
- Oncogenic K‐ras promotes early carcinogenesis in the mouse proximal colonInternational Journal of Cancer, 2008
- Epigenetic silencing of the intronic microRNA hsa-miR-342 and its host gene EVL in colorectal cancerOncogene, 2008
- Expression of Epiregulin and Amphiregulin and K-ras Mutation Status Predict Disease Control in Metastatic Colorectal Cancer Patients Treated With CetuximabJournal of Clinical Oncology, 2007
- Transforming Growth Factor-β1 Mediates Epithelial to Mesenchymal Transdifferentiation through a RhoA-dependent MechanismMolecular Biology of the Cell, 2001
- Involvement of deregulated epiregulin expression in tumorigenesis in vivo through activated Ki-Ras signaling pathway in human colon cancer cells.2000
- TGFβ Signaling in Growth Control, Cancer, and Heritable DisordersCell, 2000
- The Hallmarks of CancerCell, 2000
- Defects in transforming growth factor-β signaling cooperate with a Ras oncogene to cause rapid aneuploidy and malignant transformation of mouse keratinocytesProceedings of the National Academy of Sciences of the United States of America, 1999