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  PubMed Tumor-targeting Salmonella typhimurium A1-R Sensitizes melanoma with a BRAF-V600E Mutation to Vemurafenib in a Patient-derived Orthotopic Xenograft (PDOX) Nude Mouse Model.
 In addition, Vemurafenib (VEM) was not effective even though VEM is supposed to target the BRAF-V600E mutation.
  After several weeks of long‑term in vitro treatment of two different V600E BRAF‑mutated melanoma cell lines with MARK inhibitors, PLX4032 and/or GDC-0973, the majority of the cells died whereas some remained viable and quiescent (SUR).
  PubMed Vemurafenib and trametinib reduce expression of CTGF and IL-8 in V600EBRAF melanoma cells.
 We explored the response of V600EBRAF melanoma cells derived from surgical specimens and grown in stem cell medium to Vemurafenib and trametinib, drugs targeting the activity of V600EBRAF and MEK1/2, respectively.
  In order to minimize the toxicity of cancer drugs to immune cells and other healthy cells, an anti-BRAF V600E mutant Melanoma specific drug (PLX4032) is loaded into BPLP-PLA nanoparticles.
  This has led to the development of the combination of dabrafenib and trametinib or vemurafenib and cobimetanib for the treatment of BRAF V600E mutant melanomas.
 Dabrafenib and vemurafenib target V600E/K BRAF mutants while trametinib and cobimetanib target MEK1/2.
  Vemurafenib for BRAF(V600E)-positive metastatic papillary thyroid cancer - Authors' response.
  Vemurafenib for BRAF(V600E)-positive metastatic papillary thyroid cancer.
  We therefore determined whether mitochondria-targeted metabolism-interfering agents can effectively suppress human B-Raf(V600E) melanoma cell lines and their dabrafenib/PLX4032-resistant progenies using mitochondria-targeted carboxy-proxyl (Mito-CP) and ubiquinone (Mito-Q).
  MEK/ERK inhibition by cobimetinib suppressed MCL-1 expression/phosphorylation and induced proapoptotic BIM to a greater extent than did vemurafenib in BRAF(V600E) cell lines.
  Phase IB Study of Vemurafenib in Combination with Irinotecan and Cetuximab in Patients with Metastatic colorectal cancer with BRAFV600E Mutation.
 In vitro, EGFR inhibition, combined with the BRAF inhibitor Vemurafenib, causes synergistic cytotoxicity for BRAF(V600E) metastatic colorectal cancer, further augmented by irinotecan.
 In this 3+3 phase I study, patients with BRAF(V600E)-advanced solid cancers received cetuximab and irinotecan with escalating doses of Vemurafenib.
 Vemurafenib, in combination with irinotecan and cetuximab, was well tolerated in patients with refractory, BRAF-mutated metastatic colorectal cancer, and both survival outcomes and response rates exceeded prior reports for Vemurafenib and for irinotecan plus cetuximab in BRAF(V600E) metastatic colorectal cancer.
  PubMed Vemurafenib in combination with cobimetinib in relapsed and refractory extramedullary multiple myeloma harboring the BRAF V600E mutation.
 We here present the first report on the combination of Vemurafenib and cobimetinib in a young patient with highly resistant and rapidly progressing multiple myeloma harboring the BRAF V600E mutation who achieved a rapid and sustained response to this combination therapy.
  Inhibition of BRAFV600E using vemurafenib, independently of its cytostatic effects, suppresses metastasis by acting on the PGC1α-ID2-TCF4-integrin axis.
  MEK kinase inhibitors (trametinib and selumetinib) or kinase inhibitors directed against mutated BRAF(V600E) (vemurafenib and dabrafenib) have initial encouraging effects in the treatment of melanoma but acquired resistance appears almost invariably after some months.
  Her tumor was positive for the BRAF 1799T>A (V600E) mutation, and she was treated with BRAF inhibitor therapy (vemurafenib).
  Crizotinib has also demonstrated activity on patients with ROS1 rearrangements, and BRAF inhibitors (dabrafenib, vemurafenib) have demonstrated activity in patients with NSCLC with BRAF V600E mutation.
  Sustained Response to Vemurafenib in a BRAF(V600E)-Mutated Anaplastic Thyroid Carcinoma Patient.
  We used the BRAF inhibitor vemurafenib to treat a 53 year-old female suffering from a BRAF(V600E) mutated metastatic CMM.
  As a proof of principle, we established drug efficacy of the FDA-approved BRAF(V600E) inhibitor, Vemurafenib, in adult zebrafish harboring BRAF(V600E) melanoma tumors.
  PubMed Vemurafenib in patients with BRAF(V600E)-positive metastatic or unresectable papillary thyroid cancer refractory to radioactive iodine: a non-randomised, multicentre, open-label, phase 2 trial.
 Vemurafenib, an oncogenic BRAF kinase inhibitor approved for BRAF-positive melanoma, showed clinical benefit in three patients with BRAF(V600E)-positive papillary thyroid cancer in a phase 1 trial.
 We aimed to establish the activity of Vemurafenib in patients with BRAF(V600E)-positive papillary thyroid cancer.
 INTERPRETATION: Vemurafenib showed antitumour activity in patients with progressive, BRAF(V600E)-positive papillary thyroid cancer refractory to radioactive iodine who had never been treated with a multikinase inhibitor.
  Our cell growth assays showed that under controlled hypoxic conditions, BRAF(V600E) melanoma cells rapidly became resistant to vemurafenib.
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