Literature DB >> 25285888

BRAF inhibitor dabrafenib in patients with metastatic BRAF-mutant thyroid cancer.

Gerald S Falchook1, Michael Millward, David Hong, Aung Naing, Sarina Piha-Paul, Steven G Waguespack, Maria E Cabanillas, Steven I Sherman, Bo Ma, Martin Curtis, Vicki Goodman, Razelle Kurzrock.   

Abstract

BACKGROUND: Mutations of v-raf murine sarcoma viral oncogene homolog B (BRAF) are commonly identified in papillary and anaplastic thyroid carcinoma and are associated with worse prognosis compared with the wild type. BRAF inhibition in papillary thyroid carcinoma cell lines and xenografts inhibits proliferation and decreases downstream phosphorylation. Our objectives were to analyze safety and efficacy of the selective BRAF inhibitor dabrafenib in patients with metastatic BRAF-mutant thyroid carcinoma.
METHODS: We present the subset of patients with BRAF-mutant thyroid carcinoma enrolled in a larger phase 1 study, the main results of which are reported elsewhere.
RESULTS: Fourteen patients with BRAF(V600E)-mutant thyroid carcinoma were enrolled, of whom 13 (93%) had received prior radioactive iodine. The median duration on treatment was 8.4 months, and seven (50%) patients received treatment for ≥10 months. The most common treatment-related adverse events were skin papillomas (n=8, 57%), hyperkeratosis (n=5, 36%), and alopecia (n=4, 29%), all of which were grade 1. Treatment-related adverse events grade ≥3 included grade 4 elevated lipase and grade 3 elevated amylase, fatigue, febrile neutropenia, and cutaneous squamous cell carcinoma (n=1 for each). Four (29%) partial responses were observed, and nine (64%) patients achieved at least 10% decrease. Only one responder progressed while on the study drug after a response duration of 9.3 months. The other three responders had not progressed, with response duration of 4.6+, 10.4+, and 21.4+ months. With seven (50%) patients showing no progression at the time of study completion, the median progression-free survival was 11.3 months.
CONCLUSIONS: Dabrafenib was well tolerated and resulted in durable responses in BRAF-mutant differentiated thyroid carcinoma patients.

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Year:  2015        PMID: 25285888      PMCID: PMC4291160          DOI: 10.1089/thy.2014.0123

Source DB:  PubMed          Journal:  Thyroid        ISSN: 1050-7256            Impact factor:   6.568


  32 in total

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2.  Inhibition of mutated, activated BRAF in metastatic melanoma.

Authors:  Keith T Flaherty; Igor Puzanov; Kevin B Kim; Antoni Ribas; Grant A McArthur; Jeffrey A Sosman; Peter J O'Dwyer; Richard J Lee; Joseph F Grippo; Keith Nolop; Paul B Chapman
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3.  MEK inhibitor PD0325901 significantly reduces the growth of papillary thyroid carcinoma cells in vitro and in vivo.

Authors:  Ying C Henderson; Yunyun Chen; Mitchell J Frederick; Stephen Y Lai; Gary L Clayman
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4.  Dissecting therapeutic resistance to RAF inhibition in melanoma by tumor genomic profiling.

Authors:  Nikhil Wagle; Caroline Emery; Michael F Berger; Matthew J Davis; Allison Sawyer; Panisa Pochanard; Sarah M Kehoe; Cory M Johannessen; Laura E Macconaill; William C Hahn; Matthew Meyerson; Levi A Garraway
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5.  Phosphatidylinositol 3-kinase/akt and ras/raf-mitogen-activated protein kinase pathway mutations in anaplastic thyroid cancer.

Authors:  Libero Santarpia; Adel K El-Naggar; Gilbert J Cote; Jeffrey N Myers; Steven I Sherman
Journal:  J Clin Endocrinol Metab       Date:  2007-11-07       Impact factor: 5.958

6.  High rate of BRAF and RET/PTC dual mutations associated with recurrent papillary thyroid carcinoma.

Authors:  Ying C Henderson; Thomas D Shellenberger; Michelle D Williams; Adel K El-Naggar; Mitchell J Fredrick; Kathleen M Cieply; Gary L Clayman
Journal:  Clin Cancer Res       Date:  2009-01-15       Impact factor: 12.531

7.  Cytostatic activity of adenosine triphosphate-competitive kinase inhibitors in BRAF mutant thyroid carcinoma cells.

Authors:  Paolo Salerno; Valentina De Falco; Anna Tamburrino; Tito Claudio Nappi; Giancarlo Vecchio; Rebecca E Schweppe; Gideon Bollag; Massimo Santoro; Giuliana Salvatore
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8.  Advances in targeting the Ras/Raf/MEK/Erk mitogen-activated protein kinase cascade with MEK inhibitors for cancer therapy.

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9.  Clinicopathologic significance of BRAF V600E mutation in papillary carcinomas of the thyroid: a meta-analysis.

Authors:  Ju-Han Lee; Eung-Seok Lee; Young-Sik Kim
Journal:  Cancer       Date:  2007-07-01       Impact factor: 6.860

10.  BRAF V600E mutation in anaplastic thyroid carcinomas and their accompanying differentiated carcinomas.

Authors:  T Takano; Y Ito; M Hirokawa; H Yoshida; A Miyauchi
Journal:  Br J Cancer       Date:  2007-04-24       Impact factor: 7.640

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  51 in total

1.  The Treatment of Advanced Thyroid Cancer in the Age of Novel Targeted Therapies.

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Journal:  Drugs       Date:  2017-05       Impact factor: 9.546

2.  MAPK- and AKT-activated thyroid cancers are sensitive to group I PAK inhibition.

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3.  KRAS G12V Mutation in Acquired Resistance to Combined BRAF and MEK Inhibition in Papillary Thyroid Cancer.

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5.  BRAF-mutated clear cell sarcoma is sensitive to vemurafenib treatment.

Authors:  Svetlana A Protsenko; Anna I Semionova; Yuri I Komarov; Svetlana N Aleksakhina; Alexandr O Ivantsov; Aglaya G Iyevleva; Evgeny N Imyanitov
Journal:  Invest New Drugs       Date:  2015-08-20       Impact factor: 3.850

Review 6.  Current Standards in Treatment of Radioiodine Refractory Thyroid Cancer.

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7.  Molecular targeting of papillary thyroid carcinoma with fluorescently labeled ratiometric activatable cell penetrating peptides in a transgenic murine model.

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Review 8.  Targeting lipid metabolism for the treatment of anaplastic thyroid carcinoma.

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9.  Detection of Circulating BRAF(V600E) in Patients with Papillary Thyroid Carcinoma.

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Journal:  J Mol Diagn       Date:  2015-11-26       Impact factor: 5.568

10.  EGFR inhibition enhances the antitumor efficacy of a selective BRAF V600E inhibitor in thyroid cancer cell lines.

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