Metastasis is driven by sequential elevation of H-ras and Smad2 levels.
about
The use of cystatin C to inhibit epithelial-mesenchymal transition and morphological transformation stimulated by transforming growth factor-beta.Interaction with Smad4 is indispensable for suppression of BMP signaling by c-SkiBreast cancer bone metastasis mediated by the Smad tumor suppressor pathwaySmad7 induces hepatic metastasis in colorectal cancerThe epithelial-mesenchymal transition generates cells with properties of stem cellsSmall C-terminal domain phosphatase enhances snail activity through dephosphorylationInhibition of transforming growth factor-beta1-induced signaling and epithelial-to-mesenchymal transition by the Smad-binding peptide aptamer Trx-SARAConstitutive activation of the Ras-Raf signaling pathway in metastatic melanoma is associated with poor prognosisInduction by transforming growth factor-beta1 of epithelial to mesenchymal transition is a rare event in vitroHost microenvironment in breast cancer development: epithelial-mesenchymal transition in breast cancer developmentp19Arf suppresses growth, progression, and metastasis of Hras-driven carcinomas through p53-dependent and -independent pathwaysHER-2 overexpression differentially alters transforming growth factor-beta responses in luminal versus mesenchymal human breast cancer cellsReversible Human TGF-β Signal Shifting between Tumor Suppression and Fibro-Carcinogenesis: Implications of Smad Phospho-Isoforms for Hepatic Epithelial-Mesenchymal TransitionsThe role of endocytic Rab GTPases in regulation of growth factor signaling and the migration and invasion of tumor cellsNormal morphogenesis of epithelial tissues and progression of epithelial tumors.An Automated High-throughput Array Microscope for Cancer Cell Mechanics.Complexities of TGF-β targeted cancer therapy.TGFβ Signaling in Tumor Initiation, Epithelial-to-Mesenchymal Transition, and MetastasisTransforming Growth Factor-Beta and Oxidative Stress Interplay: Implications in Tumorigenesis and Cancer ProgressionRas promotes transforming growth factor-β (TGF-β)-induced epithelial-mesenchymal transition via a leukotriene B4 receptor-2-linked cascade in mammary epithelial cellsSmad2 and Smad3 have opposing roles in breast cancer bone metastasis by differentially affecting tumor angiogenesisInvolvement of EGF receptor and c-Src in the survival signals induced by TGF-beta1 in hepatocytesNotch promotes epithelial-mesenchymal transition during cardiac development and oncogenic transformationModulation of NFkappaB activity and E-cadherin by the type III transforming growth factor beta receptor regulates cell growth and motilityTGF-beta-induced epithelial to mesenchymal transitionNonlinear optical imaging to evaluate the impact of obesity on mammary gland and tumor stromaTargeting the transforming growth factor-beta signaling pathway in human cancer.Complete reversal of epithelial to mesenchymal transition requires inhibition of both ZEB expression and the Rho pathwayThe tale of transforming growth factor-beta (TGFbeta) signaling: a soigné enigma.Elevated cutaneous Smad activation associates with enhanced skin tumor susceptibility in organ transplant recipients.Dynamics of chromatin accessibility during TGF-β-induced EMT of Ras-transformed mammary gland epithelial cells.PAI-1 Regulates the Invasive Phenotype in Human Cutaneous Squamous Cell Carcinoma.TGF-beta and the Smad signaling pathway support transcriptomic reprogramming during epithelial-mesenchymal cell transitionDistinct mechanisms of TGF-beta1-mediated epithelial-to-mesenchymal transition and metastasis during skin carcinogenesis.Antiproliferative and proapoptotic activities of anthocyanin and anthocyanidin extracts from blueberry fruits on B16-F10 melanoma cells.Smad2 and Smad6 as predictors of overall survival in oral squamous cell carcinoma patientsPro-oncogenic and anti-oncogenic pathways: opportunities and challenges of cancer therapy.Suppression of injury-induced epithelial-mesenchymal transition in a mouse lens epithelium lacking tenascin-CCancer associated fibroblasts (CAFs) in tumor microenvironment.Epigenetic downregulation of human disabled homolog 2 switches TGF-beta from a tumor suppressor to a tumor promoter.
P2860
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P2860
Metastasis is driven by sequential elevation of H-ras and Smad2 levels.
description
2002 nî lūn-bûn
@nan
2002年の論文
@ja
2002年学术文章
@wuu
2002年学术文章
@zh-cn
2002年学术文章
@zh-hans
2002年学术文章
@zh-my
2002年学术文章
@zh-sg
2002年學術文章
@yue
2002年學術文章
@zh
2002年學術文章
@zh-hant
name
Metastasis is driven by sequential elevation of H-ras and Smad2 levels.
@en
Metastasis is driven by sequential elevation of H-ras and Smad2 levels.
@nl
type
label
Metastasis is driven by sequential elevation of H-ras and Smad2 levels.
@en
Metastasis is driven by sequential elevation of H-ras and Smad2 levels.
@nl
prefLabel
Metastasis is driven by sequential elevation of H-ras and Smad2 levels.
@en
Metastasis is driven by sequential elevation of H-ras and Smad2 levels.
@nl
P2093
P356
P1433
P1476
Metastasis is driven by sequential elevation of H-ras and Smad2 levels.
@en
P2093
Allan Balmain
Martin Oft
Rosemary J Akhurst
P2888
P304
P356
10.1038/NCB807
P577
2002-07-01T00:00:00Z
P5875
P6179
1028107107