ReviewCarcinogenesis2010
Resistance to transforming growth factor β-mediated tumor suppression in melanoma: are multiple mechanisms in place?
Review in Carcinogenesis, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 33 citations in OpenAlex.
- A positive feedback loop between SMAD3 and PINK1 in regulation of mitophagy.Cell discovery · 2025Article
- Importance of Fibrosis in the Pathogenesis of Uterine Leiomyoma and the Promising Anti-fibrotic Effects of Dipeptidyl Peptidase-4 and Fibroblast Activation Protein Inhibitors in the Treatment of Uterine Leiomyoma.Reproductive sciences (Thousand Oaks, Calif.) · 2023Review
- Vascular endothelial growth factor-C in activating vascular endothelial growth factor receptor-3 and chemokine receptor-4 in melanoma adhesion.Journal of cellular and molecular medicine · 2022Review
- Ectopic expression of the osteogenic master geneWorld journal of stem cells · 2018Article
- Grainyhead-like 2 (GRHL2) knockout abolishes oral cancer development through reciprocal regulation of the MAP kinase and TGF-β signaling pathways.Oncogenesis · 2018Article
- Systems biology analysis of mitogen activated protein kinase inhibitor resistance in malignant melanoma.BMC systems biology · 2018Article
- Nano-delivery of fraxinellone remodels tumor microenvironment and facilitates therapeutic vaccination in desmoplastic melanoma.Theranostics · 2018Article
- Targeting the hedgehog transcription factors GLI1 and GLI2 restores sensitivity to vemurafenib-resistant human melanoma cells.Oncogene · 2017Article
- Mutational activation of BRAF confers sensitivity to transforming growth factor beta inhibitors in human cancer cells.Oncotarget · 2016Article
- Article
- Mechanisms of environmental chemicals that enable the cancer hallmark of evasion of growth suppression.Carcinogenesis · 2015Review
- The leukemia inhibitory factor (LIF) and p21 mediate the TGFβ tumor suppressive effects in human cutaneous melanoma.BMC cancer · 2015Article
- In-depth genomic data analyses revealed complex transcriptional and epigenetic dysregulations of BRAFV600E in melanoma.Molecular cancer · 2015Article
- EWI-2 negatively regulates TGF-β signaling leading to altered melanoma growth and metastasis.Cell research · 2015Article
- Snowball: resampling combined with distance-based regression to discover transcriptional consequences of a driver mutation.Bioinformatics (Oxford, England) · 2015Article
- RUNX2 is overexpressed in melanoma cells and mediates their migration and invasion.Cancer letters · 2014Article
- FKBP51 increases the tumour-promoter potential of TGF-beta.Clinical and translational medicine · 2014Article
- Type III TGF-β receptor downregulation generates an immunotolerant tumor microenvironment.The Journal of clinical investigation · 2013Article
- Insights into the Transforming Growth Factor-β Signaling Pathway in Cutaneous Melanoma.Annals of dermatology · 2013Article
- Non-canonical Smads phosphorylation induced by the glutamate release inhibitor, riluzole, through GSK3 activation in melanoma.PloS one · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Resistance to transforming growth factor (TGF) β-mediated tumor suppression in melanoma appears to be a crucial step in tumor aggressiveness since it is usually coupled with the ability of TGFβ to drive the oncogenic process via autocrine and paracrine effects. In this review, we will focus mainly on the mechanisms of escape from TGFβ-induced cell cycle arrest because the mechanisms of resistance to TGFβ-mediated apoptosis are still essentially speculative. As expected, some of these mechanisms can directly affect the function of the main downstream effectors of TGFβ, Smad2 and Smad3, resulting in compromised Smad-mediated antiproliferative activity. Other mechanisms can counteract or overcome TGFβ-mediated cell cycle arrest independently of the Smads. In melanoma, some models of resistance to TGFβ have been suggested and will be described. In addition, we propose additional models of resistance taking into consideration the information available on the dysregulation of fundamental cellular effectors and signaling pathways in melanoma.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.