ArticleBiochemical and biophysical research communications2011
The BRAFT1799A mutation confers sensitivity of thyroid cancer cells to the BRAFV600E inhibitor PLX4032 (RG7204).
Article in Biochemical and biophysical research communications, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
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31 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.
- A pharmacogenomic method for individualized prediction of drug sensitivity.Molecular systems biology · 2011Pooled it
- Dabrafenib Versus Dabrafenib + Trametinib inThyroid : official journal of the American Thyroid Association · 2022Trial
- Clinical outcomes of dabrafenib plus trametinib in locally advanced or metastatic BRAF V600E-mutant papillary thyroid cancer.American journal of cancer research · 2025Article
- Low-Density Lipoprotein Receptor Is a Key Driver of Aggressiveness in Thyroid Tumor Cells.International journal of molecular sciences · 2023Article
- Nuclear interaction of Arp2/3 complex and BRAFAmerican journal of cancer research · 2022Article
- Toll-Like Receptor 7 Mediates Inflammation Resolution and Inhibition of Angiogenesis in Non-Small Cell Lung Cancer.Cancers · 2021Article
- PD-1 blockade delays tumor growth by inhibiting an intrinsic SHP2/Ras/MAPK signalling in thyroid cancer cells.Journal of experimental & clinical cancer research : CR · 2021Article
- Article
- MAPK- and AKT-activated thyroid cancers are sensitive to group I PAK inhibition.Endocrine-related cancer · 2019Article
- MAPK Inhibitors Enhance HDAC Inhibitor-Induced Redifferentiation in Papillary Thyroid Cancer Cells HarboringMolecular therapy oncolytics · 2019Article
- The MEK1/2 Inhibitor AZD6244 Sensitizes BRAF-Mutant Thyroid Cancer to Vemurafenib.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- HER inhibitor promotes BRAF/MEK inhibitor-induced redifferentiation in papillary thyroid cancer harboring BRAFV600E.Oncotarget · 2017Article
- Expression Profiling of a Human Thyroid Cell Line Stably Expressing the BRAFV600E Mutation.Cancer genomics & proteomics · 2017Article
- Dual EGFR and BRAF blockade overcomes resistance to vemurafenib in BRAF mutated thyroid carcinoma cells.Cancer cell international · 2017Article
- Pluripotency markers are differentially induced by MEK inhibition in thyroid and melanoma BRAFV600E cell lines.Cancer biology & therapy · 2016Article
- B-Raf mutation and papillary thyroid carcinoma patients.Oncology letters · 2016Article
- Robust Thyroid Gene Expression and Radioiodine Uptake Induced by Simultaneous Suppression of BRAF V600E and Histone Deacetylase in Thyroid Cancer Cells.The Journal of clinical endocrinology and metabolism · 2016Article
- Hyperactive ERK and persistent mTOR signaling characterize vemurafenib resistance in papillary thyroid cancer cells.Oncotarget · 2016Article
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Abstract
Aberrant signaling of the Ras-Raf-MEK-ERK (MAP kinase) pathway driven by the mutant kinase BRAF(V600E), as a result of the BRAF(T1799A) mutation, plays a fundamental role in thyroid tumorigenesis. This study investigated the therapeutic potential of a BRAF(V600E)-selective inhibitor, PLX4032 (RG7204), for thyroid cancer by examining its effects on the MAP kinase signaling and proliferation of 10 thyroid cancer cell lines with wild-type BRAF or BRAF(T1799A) mutation. We found that PLX4032 could effectively inhibit the MAP kinase signaling, as reflected by the suppression of ERK phosphorylation, in cells harboring the BRAF(T1799A) mutation. PLX4032 also showed a potent and BRAF mutation-selective inhibition of cell proliferation in a concentration-dependent manner. PLX4032 displayed low IC(50) values (0.115-1.156μM) in BRAF(V600E) mutant cells, in contrast with wild-type BRAF cells that showed resistance to the inhibitor with high IC(50) values (56.674-1349.788μM). Interestingly, cells with Ras mutations were also sensitive to PLX4032, albeit moderately. Thus, this study has confirmed that the BRAF(T1799A) mutation confers cancer cells sensitivity to PLX4032 and demonstrated its specific potential as an effective and BRAF(T1799A) mutation-selective therapeutic agent for thyroid cancer.
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