| Tumor suppressor and oncogene actions of TGFbeta1 occur early in skin carcinogenesis and are mediated by Smad3. | skin, |
| deregulation of c-MYC in lymphoma cells does not overcome the tumor suppressor function of TGF-beta and that repression of E2F-1 transcription is sufficient for the efficient induction of cytostasis. | lymphoma, |
| Results indicate that SKI exploits multiple regulatory levels of the TGF-beta pathway and its deficiency restores TGF-beta tumor suppressor and apoptotic activities in spite of the likely presence of oncogenic mutations in melanoma tumors. | skin, |
| TGF-beta1 induced signal transduction in hepatocytes may contribute to tumor suppression (growth inhibition and apoptosis), and to liver tumor progression and invasion (EMT and acquisition of a stem-like phenotype). | liver, |
| dysregulated TGFbeta/SMAD4 signaling may lead to epigenetic silencing of a putative tumor suppressor, RunX1T1, during ovarian carcinogenesis | ovarian, |
| Melanoma patients with a metastatic episode had less circulating TGF-beta1.Lower levels of TGF-beta1 were related to increased oxidative stress in metastasis patients. In melanoma TGF-beta1 acts as a tumor suppressor, inhibiting tumor relapse. | skin, |
| Canonical TGF-beta and c-KIT signaling forms a positive, tumor-promoting feedback loop. Disruption of this loop restores TGF-beta tumor suppressor function and provides the rationale for targeting the TGF-beta/SCF axis as a novel therapeutic strategy for Hepatocellular carcinoma. | liver, |
| In this review, we discuss the effects of TGFb-driven transcription on all stages of tumour progression, with special focus on lung cancer. Since some TGFb target genes are specifically involved in promoting metastasis, we speculate that these genes might be good targets to block tumour progression without compromising the tumour suppressor effects of the TGFb pathway. | lung, |
| The tumor suppressive TGF-?/SMAD1/S1PR2 signaling axis is recurrently inactivated in diffuse large B-cell lymphoma | lymphoma, |
| Epigenetic suppression of TPM1 may alter TGF-beta tumor suppressor function and contribute to metastatic properties of tumor cells. | None |
| May modulate its own signalling to facilitate switching from tumour suppression to tumour progression. | None |
| Studies provide the first evidence that TGFBI functions as a tumor suppressor in vivo. | None |
| High levels of Smad3 are required for the tumor suppressor activities of TGF-beta, whereas lower levels are sufficient for the tumor promoting functions. | None |
| analysis of a novel TGFbeta/PKA tumor suppressor pathway that acts directly on a known cell survival mechanism that responds to stress with the survivin/XIAP dependent inhibition of caspases that effect apoptosis | None |
| our findings indicate that alphavbeta6 and TGF-beta act in a common tumor suppressor pathway | None |
| The present study indicates that TGFB1 variants have subtype-specific roles in BC and may switch from tumor suppressor to promoter during tumor development, consistent with TGFbeta1 dual role in BC pathogenesis. | None |
| Transforming growth factor-beta1 is a new form of tumor suppressor with true haploid insufficiency. | None |
| TGF-beta is a modulator of beta-Catenin levels in tumoral fibroblasts and non-tumoral fibroblasts, despite the oncogenic mutations already present in this gene in tumoral fibroblasts of desmoid tumors. | oral |
| Sphingosine kinases and sphingosine-1-phosphate are critical for transforming growth factor beta-induced extracellular signal-regulated kinase 1 and 2 activation and promotion of migration and invasion of esophageal cancer cells. | esophageal, |
| Tumor suppressor and oncogene actions of TGFbeta1 occur early in skin carcinogenesis and are mediated by Smad3. | skin, |