In vivo MAPK reporting reveals the heterogeneity in tumoral selection of resistance to RAF inhibitors
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Summary
A novel ERK1/2 reporter system is reported that provides a non-invasive, quantitative and temporal analysis of RAF inhibitor efficacy in vivo and reveals heterogeneity in the level of ERK1/2 reactivation associated with acquired resistance to RAF inhibition.
- Type
- article
- Published
- 2013-10-11
- Cited by
- 32
- References
- 24
- Access
- Open access
- OpenAlex
- https://openalex.org/W2011261819
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:10331770
Keywords
In vivo, Selection (genetic algorithm), Resistance (ecology), Cancer research, Biology
References
- PLX4032, a selective BRAFV600E kinase inhibitor, activates the ERK pathway and enhances cell migration and proliferation of BRAFWT melanoma cells
- Nuclear localization and regulation of erk- and rsk-encoded protein kinases
- Clinical efficacy of a RAF inhibitor needs broad target blockade in BRAF-mutant melanoma
- SHOC2 and CRAF Mediate ERK1/2 Reactivation in Mutant NRAS-mediated Resistance to RAF Inhibitor*
- Progression of RAS-Mutant Leukemia during RAF Inhibitor Treatment
- The SRF accessory protein Elk-1 contains a growth factor-regulated transcriptional activation domain.
- Concurrent loss of the PTEN and RB1 tumor suppressors attenuates RAF dependence in melanomas harboring V600EBRAF
- 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.
- BH3-only protein silencing contributes to acquired resistance to PLX4720 in human melanoma
- Melanomas acquire resistance to B-RAF(V600E) inhibition by RTK or N-RAS upregulation
- RAF inhibitor resistance is mediated by dimerization of aberrantly spliced BRAF(V600E)
- Cyclin D3 Expression in Melanoma Cells Is Regulated by Adhesion-dependent Phosphatidylinositol 3-Kinase Signaling and Contributes to G1-S Progression*
- FOXD3 is a mutant B-RAF-regulated inhibitor of G1/S progression in melanoma cells
- Melanoma whole exome sequencing identifies V600EB-RAF amplification-mediated acquired B-RAF inhibitor resistance
- Modelling vemurafenib resistance in melanoma reveals a strategy to forestall drug resistance
- Phase II study of the MEK1/MEK2 inhibitor Trametinib in patients with metastatic BRAF-mutant cutaneous melanoma previously treated with or without a BRAF inhibitor.
- Kinase-Dead BRAF and Oncogenic RAS Cooperate to Drive Tumor Progression through CRAF
- Discovery of a selective inhibitor of oncogenic B-Raf kinase with potent antimelanoma activity
- Combined BRAF and MEK Inhibition in Melanoma with BRAF V600 Mutations
Cited by
- E-cadherin knockdown increases β-catenin reducing colorectal cancer chemosensitivity only in three-dimensional cultures.
- The RAF-MEK-ERK pathway: targeting ERK to overcome obstacles to effective cancer therapy.
- Inhibition of mutant BRAF splice variant signaling by next generation, selective RAF inhibitors
- Non-BRAF-targeted therapy, immunotherapy, and combination therapy for melanoma
- Fibroblast-derived Neuregulin 1 Promotes Compensatory ErbB3 Receptor Signaling in Mutant BRAF Melanoma*
- Beneficial Effects of RAF Inhibitor in Mutant BRAF Splice Variant-expressing Melanoma
- Somatic DNA mutation analysis in targeted therapy of solid tumours.
- Of Mice and Melanoma
- The transcription factor RUNX2 regulates receptor tyrosine kinase expression in melanoma
- Asparagine promotes cancer cell proliferation through use as an amino acid exchange factor
- An in vivo reporter to quantitatively and temporally analyze the effects of CDK4/6 inhibitor-based therapies in melanoma
- Combined BRAFV600E and MEK blockade for BRAFV600E-mutant gliomas
- Context-dependent miR-204 and miR-211 affect the biological properties of amelanotic and melanotic melanoma cells
- SOX2 regulates multiple malignant processes of breast cancer development through the SOX2/miR-181a-5p, miR-30e-5p/TUSC3 axis
- Methylation of SLFN11 is a marker of poor prognosis and cisplatin resistance in colorectal cancer.
- Response and resistance to paradox breaking BRAF inhibitor in melanomas in vivo and ex vivo
- Arrested developments: CDK4/6 inhibitor resistance and alterations in the tumor immune microenvironment
- BRAF Splice Variant Resistance to RAF Inhibitor Requires Enhanced MEK Association
- Targeting the CINful genome: Strategies to overcome tumor heterogeneity.
- CADM1 is a TWIST1-regulated suppressor of invasion and survival
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