Induction of EMT by Twist Proteins as a Collateral Effect of Tumor-Promoting Inactivation of Premature Senescence
- 1 July 2008
- journal article
- research article
- Published by Elsevier BV in Cancer Cell
- Vol. 14 (1), 79-89
- https://doi.org/10.1016/j.ccr.2008.06.005
Abstract
No abstract availableKeywords
This publication has 40 references indexed in Scilit:
- Systemic Spread Is an Early Step in Breast CancerCancer Cell, 2008
- Knock-in of Mutant K-ras in Nontumorigenic Human Epithelial Cells as a New Model for Studying K-ras–Mediated TransformationCancer Research, 2007
- Molecular characterization of the t(3;9) associated with immortalization in the MCF10A cell lineCancer Genetics and Cytogenetics, 2005
- Genomic analysis of single cytokeratin-positive cells from bone marrow reveals early mutational events in breast cancerCancer Cell, 2005
- BRAFE600-associated senescence-like cell cycle arrest of human naeviNature, 2005
- Senescence in premalignant tumoursNature, 2005
- Activation of the DNA damage checkpoint and genomic instability in human precancerous lesionsNature, 2005
- DNA damage response as a candidate anti-cancer barrier in early human tumorigenesisNature, 2005
- Oncogenic cooperation between H-Twist and N-Myc overrides failsafe programs in cancer cellsCancer Cell, 2004
- The M-twist gene of Mus is expressed in subsets of mesodermal cells and is closely related to the Xenopus X-twi and the Drosophila twist genesDevelopmental Biology, 1991