See JNCCN.org for supplemental online content.
Dr. Solomon has disclosed that he receives grant/research support from and is on the advisory board for Novartis AG. The remaining authors have disclosed that they have no financial interests, arrangements, affiliations, or commercial interests with the manufacturers of any products discussed in this article or their competitors.
SmallridgeRCAinKBAsaSL. American Thyroid Association guidelines for management of patients with anaplastic thyroid cancer. Thyroid2012;22:1104–1139.
HowladerNNooneAMKrapchoM eds. SEER Cancer Statistics Review 1975-2012National Cancer Institute. Bethesda, MD. Available at: http://seer.cancer.gov/csr/1975_2012/based on November 2014 SEER data submission posted to the SEER web site April 2015. Accessed February 4 2016.
DenaroNNigroCLRussiEGMerlanoMC. The role of chemotherapy and latest emerging target therapies in anaplastic thyroid cancer. Onco Targets Ther2013;9:1231–1241.
Ricarte-FilhoJCRyderMChitaleDA. Mutational profile of advanced primary and metastatic radioactive iodine-refractory thyroid cancers reveals distinct pathogenetic roles for BRAF, PIK3CA, and AKT1. Cancer Res2009;69:4885–4893.
SmallridgeRCMarlowLACoplandJA. Anaplastic thyroid cancer: molecular pathogenesis and emerging therapies. Endocr Relat Cancer2009;16:17–44.
BegumSRosenbaumEHenriqueR. BRAF mutations in anaplastic thyroid carcinoma: implications for tumor origin, diagnosis and treatment. Mod Pathol2004;17:1359–1363.
JohannessenCMBoehmJSKimSY. COT drives resistance to RAF inhibition through MAP kinase pathway reactivation. Nature2010;468:968–972.
NazarianRShiHWangQ. Melanomas acquire resistance to B-RAF(V600E) inhibition by RTK or N-RAS upregulation. Nature2010;468:973–977.
PoulikakosPIPersaudYJanakiramanM. RAF inhibitor resistance is mediated by dimerization of aberrantly spliced BRAF(V600E). Nature2011;480:387–390.
ThakurMDStuartDD. Molecular pathways: response and resistance to BRAF and MEK inhibitors in BRAFV600E Tumors. Clin Cancer Res2014;20:1074–1080.
Montero-CondeCRuiz-LlorenteSDominguezJM. Relief of feedback inhibition of HER3 transcription by RAF and MEK inhibitors attenuates their antitumor effects in BRAF-mutant thyroid carcinomas. Cancer Discov2013;3:520–533.
LongGVStroyakovskiyDGogasH. Combined BRAF and MEK inhibition versus BRAF inhibition alone in melanoma. N Engl J Med2014;371:1877–1888.
MitsiadesCSNegriJMcMullanC. Targeting BRAFV600E in thyroid carcinoma: therapeutic implications. Molecular cancer therapeutics2007;6:1070–1078.
TakanoTItoYHirokawaM. BRAFV600E mutation in anaplastic thyroid carcinomas and their accompanying differentiated carcinomas. Br J Cancer2007;96:1549–1553.
RagazziMCiarrocchiASancisiV. Update on anaplastic thyroid carcinoma: morphological, molecular, and genetic features of the most aggressive thyroid cancer. Int J Endocrinol2014;2014:790834.
GuerraASapioMRMarottaV. The primary occurrence of BRAF(V600E) is a rare clonal event in papillary thyroid carcinoma. J Clin Endocrinol Metab2012;97:517–524.
QuirosRMDingHGGattusoP. Evidence that one subset of anaplastic thyroid carcinomas are derived from papillary carcinomas due to BRAF and p53 mutations. Cancer2005;103:2261–2268.
XingMAlzahraniASCarsonKA. Association between BRAF V600E mutation and recurrence of papillary thyroid cancer. J Clin Oncol2015;33:42–50.
KimKBCabanillasMELazarAJ. Clinical responses to vemurafenib in patients with metastatic papillary thyroid cancer harboring BRAF(V600E) mutation. Thyroid2013;23:1277–1283.
FalchookGSLongGVKurzrockR. Dabrafenib in patients with melanoma, untreated brain metastases, and other solid tumors: a phase 1 dose-escalation trial. Lancet2012;379:1893–1901.
McArthurGAPuzanovIAmaravadiR. Marked, homogeneous, and early [18F]fluorodeoxyglucose-positron emission tomography responses to vemurafenib in BRAF-mutant advanced melanoma. J Clin Oncol2012;30:1628–1634.
McFaddenDGVernonASantiagoPM. p53 constrains progression to anaplastic thyroid carcinoma in a Braf-mutant mouse model of papillary thyroid cancer. Proc Natl Acad Sci U S A2014;111:E1600–1609.
PitaJMFigueiredoIFMouraMM. Cell cycle deregulation and TP53 and RAS mutations are major events in poorly differentiated and undifferentiated thyroid carcinomas. J Clin Endocrinol Metab2014;99:E497–507.
DonghiRLongoniAPilottiS. Gene p53 mutations are restricted to poorly differentiated and undifferentiated carcinomas of the thyroid gland. J Clin Invest1993;91:1753–1760.
FaginJAMatsuoKKarmakarA. High prevalence of mutations of the p53 gene in poorly differentiated human thyroid carcinomas. J Clin Invest1993;91:179–184.
BlagosklonnyMVGiannakakouPWojtowiczM. Effects of p53-expressing adenovirus on the chemosensitivity and differentiation of anaplastic thyroid cancer cells. J Clin Endocrinol Metab1998;83:2516–2522.
GauchotteGPhilippeCLacommeS. BRAF, p53 and SOX2 in anaplastic thyroid carcinoma: evidence for multistep carcinogenesis. Pathology2011;43:447–452.
PastoreYJedlickovaKGuanY. Mutations of von Hippel-Lindau tumor-suppressor gene and congenital polycythemia. Am J Hum Genet2003;73:412–419.