Phenotype Switching in Melanoma: Implications for Progression and Therapy
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Summary
Recent research on the role of signaling pathways and transcription factors regulating EMT-like processes in melanoma and their association with response to therapy in patients is examined, especially response to BRAF inhibition, which is initially effective but limited by development of resistance and subsequent progression.
- Type
- review
- Published
- 2015-02-13
- Cited by
- 162
- References
- 82
- Access
- Open access
- OpenAlex
- https://openalex.org/W1969621613
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:6500428
Keywords
Melanoma, Phenotype, Cancer research, Epithelial–mesenchymal transition, Metastasis
References
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- A new twist for the tumour suppressor hamartin
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- Differential LEF1 and TCF4 expression is involved in melanoma cell phenotype switching
- Cancer stem cells versus phenotype‐switching in melanoma
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- Insulin-like growth factor-1 receptor in uveal melanoma: a predictor for metastatic disease and a potential therapeutic target.
- Epithelial-mesenchymal transitions in development and disease.
- An EMT spectrum defines an anoikis-resistant and spheroidogenic intermediate mesenchymal state that is sensitive to e-cadherin restoration by a src-kinase inhibitor, saracatinib (AZD0530)
- A switch in the expression of embryonic EMT-inducers drives the development of malignant melanoma.
- HGF induces fibronectin matrix synthesis in melanoma cells through MAP kinase-dependent signaling pathway and induction of Egr-1
- MITF: master regulator of melanocyte development and melanoma oncogene.
- Melanoma Cells Revive an Embryonic Transcriptional Network to Dictate Phenotypic Heterogeneity
- The advantage of women in cancer survival: an analysis of EUROCARE-4 data.
- Functional gene expression analysis uncovers phenotypic switch in aggressive uveal melanomas.
- MED12 Controls the Response to Multiple Cancer Drugs through Regulation of TGF-β Receptor Signaling
- Targeting cancer stem cells by inhibiting Wnt, Notch, and Hedgehog pathways
- Epidermal growth factor facilitates melanoma lymph node metastasis by influencing tumor lymphangiogenesis.
- DIRECT EVIDENCE FOR A ROLE OF β‐CATENIN/LEF‐1 SIGNALING PATHWAY IN INDUCTION OF EMT
- Transcriptional Activation of ZEB1 by Slug Leads to Cooperative Regulation of the EMT like Phenotype in Melanoma
Cited by
- Editorial: Cellular and Phenotypic Plasticity in Cancer
- JUN dependency in distinct early and late BRAF inhibition adaptation states of melanoma
- Combination Therapies to Inhibit the RAF/MEK/ERK Pathway in Melanoma: We are not Done Yet
- The paradoxical role of IL-10 in immunity and cancer.
- Acid Ceramidase in Melanoma
- Adaptive immune resistance: How cancer protects from immune attack
- MITF and c-Jun antagonism interconnects melanoma dedifferentiation with pro-inflammatory cytokine responsiveness and myeloid cell recruitment
- Effects of a novel Nodal-targeting monoclonal antibody in melanoma
- Diagnosis and therapies with miRNAs in pancreatic ductal adenocarcinoma
- Modeling continuum of epithelial mesenchymal transition plasticity.
- Phenotypic tumour cell plasticity as a resistance mechanism and therapeutic target in melanoma.
- The transcription cofactor c-JUN mediates phenotype switching and BRAF inhibitor resistance in melanoma
- Dissecting the multicellular ecosystem of metastatic melanoma by single-cell RNA-seq
- Cross-talk between Dopachrome Tautomerase and Caveolin-1 Is Melanoma Cell Phenotype-specific and Potentially Involved in Tumor Progression*
- The Response of microRNAs to Solar UVR in Skin-Resident Melanocytes Differs between Melanoma Patients and Healthy Persons
- NK Cells, Tumor Cell Transition, and Tumor Progression in Solid Malignancies: New Hints for NK-Based Immunotherapy?
- Proteomics approaches to understanding mitogen-activated protein kinase inhibitor resistance in melanoma
- The Role ofBone Morphogenetic Protein Signallingin Adult Lung Health and Disease
- The prognostic potential of alternative transcript isoforms across human tumors
- Unravelling molecular mechanisms underlying therapy resistance in cutaneous melanoma
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