Resistance to BRAF inhibitors: Unraveling mechanisms and future treatment options
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Summary
Recent pre-clinical studies providing insight into the molecular mechanisms of resistance to BRAF inhibitors are reviewed and potential strategies to treat drug resistant melanomas are discussed.
- Type
- review
- Published
- 2011-12-01
- Cited by
- 160
- References
- 22
- Access
- Open access
- OpenAlex
- https://openalex.org/W2011540855
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:16616252
Keywords
Melanoma, Medicine, MAPK/ERK pathway, Cancer, Acquired resistance
References
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- RG7204 (PLX4032), a selective BRAFV600E inhibitor, displays potent antitumor activity in preclinical melanoma models.
- Clinical efficacy of a RAF inhibitor needs broad target blockade in BRAF-mutant melanoma
- Akt3-mediated resistance to apoptosis in B-RAF-targeted melanoma cells
- RAF inhibitors transactivate RAF dimers and ERK signaling in cells with wild-type BRAF
- Dissecting therapeutic resistance to RAF inhibition in melanoma by tumor genomic profiling.
- Melanomas acquire resistance to B-RAF(V600E) inhibition by RTK or N-RAS upregulation
- Targeting BRAF in advanced melanoma: a first step towards manageable disease
- RAF inhibitors prime wild-type RAF to activate the MAPK pathway and enhance growth
- Mutations in GNA11 in Uveal Melanoma
- Acquired resistance to BRAF inhibitors mediated by a RAF kinase switch in melanoma can be overcome by co-targeting MEK and IGF-1R/PI3K
- Inhibition of Mutated, Activated BRAF in Metastatic Melanoma
- Improved Survival with Vemurafenib in Melanoma with BRAF V600E Mutation
- Hyperactivation of MEK-ERK1/2 signaling and resistance to apoptosis induced by the oncogenic B-RAF inhibitor, PLX4720, in mutant N-RAS melanoma cells
- Kinase-Dead BRAF and Oncogenic RAS Cooperate to Drive Tumor Progression through CRAF
- Demonstration of a genetic therapeutic index for tumors expressing oncogenic BRAF by the kinase inhibitor SB-590885.
- Mutations of the BRAF gene in human cancer
- Faculty Opinions recommendation of COT drives resistance to RAF inhibition through MAP kinase pathway reactivation.
Cited by
- Aberrant Expression of COT Is Related to Recurrence of Papillary Thyroid Cancer
- Identifying associations between genomic alterations in tumors.
- 1.分子標的治療薬:これからの展望
- Intratumoral Heterogeneity as a Therapy Resistance Mechanism: Role of Melanoma Subpopulations
- Current management of advanced melanoma: a transformed landscape
- Other targeted drugs in melanoma.
- PTEN regulates IGF‐1R‐mediated therapy resistance in melanoma
- Automated tracking of nanoparticle-labeled melanoma cells improves the predictive power of a brain metastasis model.
- BRAF Inhibition Stimulates Melanoma-Associated Macrophages to Drive Tumor Growth
- Intravital Imaging Reveals How BRAF Inhibition Generates Drug-Tolerant Microenvironments with High Integrin β1/FAK Signaling
- Therapy’s Shadow: A Short History of the Study of Resistance to Cancer Chemotherapy
- Perturbation Biology: Inferring Signaling Networks in Cellular Systems
- Switching from MAPK-dependent to MAPK-independent repression of the sodium-iodide symporter in 2D and 3D cultured normal thyroid cells.
- Management of primary cutaneous and metastatic melanoma.
- PET Imaging of Very Late Antigen-4 in Melanoma: Comparison of 68Ga- and 64Cu-Labeled NODAGA and CB-TE1A1P-LLP2A Conjugates
- Heat-shock proteins-based immunotherapy for advanced melanoma in the era of target therapies and immunomodulating agents
- Intermittent BRAF‐inhibitor therapy is a feasible option: report of a patient with metastatic melanoma
- Uveal melanoma prognostication: from lesion size and cell type to molecular class.
- SC-535, a Novel Oral Multikinase Inhibitor, Showed Potent Antitumor Activity in Human Melanoma Models
- BRAF Inhibitors: Experience in Thyroid Cancer and General Review of Toxicity
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