ライフサイエンスコーパス: thyroid carcinoma

1 tients died of causes unrelated to medullary thyroid carcinoma).

2 cinoma (PTC) is the most common histotype of thyroid carcinoma.

3 TT cell line, derived from a human medullary thyroid carcinoma.

4 CREB5 in cholangiocarcinoma and PPL-NTRK1 in thyroid carcinoma.

5 linical promise in the treatment of advanced thyroid carcinoma.

6 hyperplasia progresses slowly to follicular thyroid carcinoma.

7 ular targets for therapeutic intervention in thyroid carcinoma.

8 verexpressed in many cancer types, including thyroid carcinoma.

9 ation previously found in familial medullary thyroid carcinoma.

10 ioiodide imaging and therapeutic ablation of thyroid carcinoma.

11 inoma, bladder cancer, low-grade glioma, and thyroid carcinoma.

12 Of the 93 patients, 57 (61%) had papillary thyroid carcinoma.

13 by 131I therapy for papillary and follicular thyroid carcinoma.

14 ed in multiple cancers, including follicular thyroid carcinoma.

15 nts after a thyroidectomy for differentiated thyroid carcinoma.

16 near-total thyroidectomy for differentiated thyroid carcinoma.

17 icacy of sorafenib in patients with advanced thyroid carcinoma.

18 anscription factors have not been studied in thyroid carcinoma.

19 asia types 2A and 2B, and familial medullary thyroid carcinoma.

20 ites of distant metastasis in differentiated thyroid carcinoma.

21 ive RET mutant, RET/PTC1, found in papillary thyroid carcinoma.

22 for the metastatic progression of papillary thyroid carcinoma.

23 mutation is frequently detected in papillary thyroid carcinoma.

24 th the risk of developing sporadic medullary thyroid carcinoma.

25 oto-oncogene could prevent or cure medullary thyroid carcinoma.

26 major weapon in the fight against metastatic thyroid carcinoma.

27 2A (MEN-2A) or type 2B or familial medullary thyroid carcinoma.

28 efficacy of 131I therapy for differentiated thyroid carcinoma.

29 ging evidence of lung cancer; 3 had renal or thyroid carcinoma.

30 the mass suggested a diagnosis of papillary thyroid carcinoma.

31 stomach carcinoma, and thyroglobulin (TG) in thyroid carcinoma.

32 dine therapy in patients with differentiated thyroid carcinoma.

33 nt of suspected recurrence of differentiated thyroid carcinoma.

34 y to illustrate the evolutionary features of thyroid carcinoma.

35 moking)-is associated with increased risk of thyroid carcinoma.

36 e metastases in patients with differentiated thyroid carcinoma.

37 actor, erythroid 2 like 2 (NFE2L2) fusion in thyroid carcinoma.

38 rrangements found in radio-induced papillary thyroid carcinoma.

39 is an extremely rare condition in papillary thyroid carcinoma.

40 virtually all of them will develop medullary thyroid carcinoma.

41 y in BRAF-mutated and MET-addicted papillary thyroid carcinomas.

42 ied and overexpressed in papillary renal and thyroid carcinomas.

43 lymphocytic and myeloblastic leukemias, and thyroid carcinomas.

44 re one of the genetic hallmarks of papillary thyroid carcinomas.

45 cluding those derived from breast, colon and thyroid carcinomas.

46 pituitary anterior lobe tumors and medullary thyroid carcinomas.

47 T tyrosine kinase commonly seen in papillary thyroid carcinomas.

48 d to be tumor-initiating events in papillary thyroid carcinomas.

49 lasms, including colon, breast, ovarian, and thyroid carcinomas.

50 ly regulate Apo2L/TRAIL-induced apoptosis in thyroid carcinomas.

51 T proto-oncogene detected in human papillary thyroid carcinomas.

52 ET/PTC3Fhit-/- mice did not develop advanced thyroid carcinomas.

53 genic RAS mutations are present in 15-30% of thyroid carcinomas.

54 e the most common type counting 86.4% of all thyroid carcinomas.

55 e performed on 148 consecutive patients with thyroid carcinoma (125 papillary, 2 follicular, 8 Hurthl

56 Molecular profiles of 11 papillary thyroid carcinomas, 13 follicular variant of papillary t

57 d follicular epithelial cells and follicular thyroid carcinoma 133 (FTC133) cells.

58 6%), lung squamous cell carcinoma (2.3%) and thyroid carcinoma (8.7%), suggesting a potential for app

59 ly mutated malignant subtypes were medullary thyroid carcinoma (9/12, 75%) and PTC (14/30, 47%).

60 rcinomas, 13 follicular variant of papillary thyroid carcinomas, 9 follicular thyroid carcinomas, and

61 Medullary thyroid carcinoma accounts for 2% to 5% of thyroid malig

62 a 7-d period in 15 patients with metastatic thyroid carcinoma after administration of (124)I-NaI.

63 oped in a patient with metastatic anaplastic thyroid carcinoma after an extraordinary 18-month respon

64 who received radioiodine for differentiated thyroid carcinoma also showed interstitial pneumonia on

65 hemical evidence of recurrent differentiated thyroid carcinoma and a tumor-negative neck US, the high

66 ssion and the oncogenic activation of RET in thyroid carcinoma and describe the involved signal trans

67 V/PV) mice) spontaneously develop follicular thyroid carcinoma and distant metastases similar to huma

68 and neck squamous cell carcinoma, melanoma, thyroid carcinoma and endometrial carcinoma).

69 ous melanomas, cutaneous nevi, and papillary thyroid carcinoma and in a small fraction of other cance

70 ter understanding of the correlation between thyroid carcinoma and LFS, tumor profile data of Brazili

71 n human cancers, including familial medullar thyroid carcinoma and multiple endocrine neoplasias 2A a

72 gement of patients with metastatic medullary thyroid carcinoma and other CCK2R-expressing malignancie

73 N 2 syndromes are characterized by medullary thyroid carcinoma and other endocrinopathies.

74 The review focuses first on medullary thyroid carcinoma and performing prophylactic thyroidect

75 he increased expression of CAIX in medullary thyroid carcinoma and provide a rationale for therapy si

76 el CREB3L2-PPARgamma gene fusion mutation in thyroid carcinoma and reveal a thyroid signaling pathway

77 y generated a transgenic mouse model of PPFP thyroid carcinoma and showed that feeding the PPARgamma

78 ified as a gene fused to the ret oncogene in thyroid carcinoma and subsequently as a co-activator for

79 ere found in follicular variant of papillary thyroid carcinomas and follicular adenomas.

80 We characterized CSCs in thyroid carcinomas and generated clones of CSC lines.

81 n which is frequently expressed in papillary thyroid carcinomas and has been detected in thyroid tiss

82 overexpressed in many cancer types including thyroid carcinomas and has well established roles in tum

83 tein, not only in FTCs but also in papillary thyroid carcinomas and Hurthle cell carcinomas.

84 in hairy-cell leukemia, cutaneous melanoma, thyroid carcinomas and, less commonly, in ovarian, colon

85 econdary breast carcinoma, 15% for secondary thyroid carcinoma, and 13% for secondary soft-tissue sar

86 e pancreatitis, pancreatic cancer, medullary thyroid carcinoma, and serious adverse events did not di

87 f papillary thyroid carcinomas, 9 follicular thyroid carcinomas, and 26 benign tumors (follicular ade

88 SNAI1 and SNAI2 are ectopically expressed in thyroid carcinomas, and aberrant expression in mice is a

89 ncogene, which is common in human follicular thyroid carcinomas appears to act via dominant negative

90 Thyroid carcinomas are fairly uncommon and include disea

91 Thyroid carcinomas are known to harbor oncogenic driver

92 Differentiated thyroid carcinomas are the most frequent endocrine neopl

93 to the widely prevalent well-differentiated thyroid carcinomas are unclear.

94 nts with progressive or metastatic medullary thyroid carcinoma, as well as other advanced-stage CCK2R

95 (SPECT/CT) on nodal staging of patients with thyroid carcinoma at the first ablative radioiodine ther

96 dmitted for adjuvant RITh for differentiated thyroid carcinoma at the University Hospital of Cologne

97 roteasome inhibitor bortezomib on anaplastic thyroid carcinoma (ATC) characterized by complete refrac

98 Anaplastic thyroid carcinoma (ATC) has among the worst prognoses of

99 Anaplastic thyroid carcinoma (ATC) is a frequently lethal malignanc

100 Anaplastic thyroid carcinoma (ATC) is a highly aggressive form of t

101 Anaplastic thyroid carcinoma (ATC) is one of the most lethal malign

102 Anaplastic thyroid carcinoma (ATC) is refractory to radioiodine the

103 ion is approximately 0.8 nM while anaplastic thyroid carcinoma (ATC) tumor growth was inhibited three

104 The increase in thyroid carcinoma, attributable to the very large amount

105 patients with meningioma, Hodgkin lymphoma, thyroid carcinoma, basal cell carcinoma, and parotid gla

106 sensus about classification and treatment of thyroid carcinoma based on standard histopathological an

107 ith suspected recurrence from differentiated thyroid carcinoma, based on an increased thyroglobulin (

108 sed after a thyroidectomy for differentiated thyroid carcinoma because it has been reported to reduce

109 y detected BRAF mutations in human papillary thyroid carcinomas (BRAF(V600E)) in thyroid follicular c

110 3 is widely expressed in well-differentiated thyroid carcinomas, but not in normal thyrocytes and ben

111 nd samples of human follicular and papillary thyroid carcinoma by reverse transcriptase-polymerase ch

112 ment in roughly one quarter of patients with thyroid carcinoma by upstaging or downstaging their dise

113 E-Cadherin (CDH1) expression is reduced in thyroid carcinomas by primarily unknown mechanisms.

114 Although CAXII was present in all types of thyroid carcinomas, CAIX, a direct HIF target implicated

115 example, anaplastic or poorly differentiated thyroid carcinoma) carry several complex genetic alterat

116 red by FOXE1 and PTCSC2 in a human papillary thyroid carcinoma cell line (KTC-1) and unaffected thyro

117 Depletion of REGgamma in a thyroid carcinoma cell line results in cell-cycle and pr

118 tary tumor, breast carcinoma cell lines, and thyroid carcinoma cell lines showed that in cells expres

119 y (BcPAP) and anaplastic (CAL62 and FRO82-1) thyroid carcinoma cell lines were characterized via West

120 f migration in both papillary and follicular thyroid carcinoma cell lines.

121 g growth factor-beta1 (TGF-beta1), papillary thyroid carcinoma cells acquired increased cancer stem c

122 els for the evaluation of IDO1 expression in thyroid carcinoma cells and for the study of involved si

123 Thyroid carcinoma cells harboring activated RET/PTC, RAS

124 ssion pattern was recapitulated in medullary thyroid carcinoma cells in vivo, consistent with a growt

125 Results: The thyroid carcinoma cells investigated were invariably gal

126 The mechanism of how IFNgamma sensitized thyroid carcinoma cells to TRAIL-induced apoptosis was i

127 The thyroid carcinoma cells were inoculated into the left th

128 regulating Apo2L/TRAIL-induced apoptosis in thyroid carcinoma cells, as well as the impact of insuli

129 in normal thyroid epithelial and follicular thyroid carcinoma cells, respectively.

130 d-type B-RAF melanoma cells and mutant B-RAF thyroid carcinoma cells.

131 electively kills neoplastic cells, including thyroid carcinoma cells.

132 of 96.2% (3 follicular variant of papillary thyroid carcinomas clustered with the benign lesions).

133 In papillary thyroid carcinomas, COMET was part of a coexpression net

134 A subset of thyroid carcinomas contains a t(2;3)(q13;p25) chromosoma

135 mPTC has become the most common form of thyroid carcinoma detected during thyroidectomies in Chi

136 Thyroid carcinoma development was analyzed in CombitTA-S

137 Recent advances in the knowledge of thyroid carcinomas development identified receptor tyros

138 PTC and anaplastic thyroid carcinomas did not show significant down-regulat

139 at stratifying patients with differentiated thyroid carcinoma (DTC) into prognostic risk groups.

140 verall prognosis in pediatric differentiated thyroid carcinoma (DTC) is excellent.

141 g recurrence or metastases in differentiated thyroid carcinoma (DTC) patients with elevated serum thy

142 Differentiated thyroid carcinoma (DTC), as one of the major component c

143 ar mortality in patients with differentiated thyroid carcinoma (DTC).

144 t PRRX1 plays an important role in papillary thyroid carcinoma EMT and disease progression.

145 vidence of persistent or recurrent medullary thyroid carcinoma five or more years after total thyroid

146 study, we have shown that familial medullary thyroid carcinoma (FMTC) mutants RET(Y791F) and RET(S891

147 e cause MEN2A, MEN2B, and familial medullary thyroid carcinoma (FMTC).

148 encies of two of the most common subtypes of thyroid carcinoma, follicular (FTC) and papillary (PTC),

149 hat 1 of 10 thyroid cancer lines [follicular thyroid carcinoma FTC-133] had hemizygous deletion and a

150 Follicular thyroid carcinoma (FTC) frequently harbors the PAX8/PPAR

151 suffering from bone metastases of follicular thyroid carcinoma (FTC) have a poor prognosis because of

152 implicated in the pathogenesis of follicular thyroid carcinoma (FTC), where a translocation with PAX8

153 llary thyroid carcinoma (PTC) and follicular thyroid carcinoma (FTC).

154 (BHD-origin renal cell carcinoma UOK257 and thyroid carcinoma FTC133) but not in their folliculin ex

155 A patient with papillary thyroid carcinoma had stable disease for more than 2 yea

156 oactive iodine ((131)I) for the treatment of thyroid carcinoma has changed over the past 50 y.

157 with a wide variety of tumors; nevertheless, thyroid carcinoma has not been evaluated in this syndrom

158 to formulate a consensus about treatment of thyroid carcinoma have resulted in published guidelines

159 naplastic or poorly differentiated recurrent thyroid carcinomas have a very poor prognosis with a med

160 ocally advanced and/or metastatic anaplastic thyroid carcinoma in a phase II cohort of the study.

161 To determine the frequency of thyroid carcinoma in Brazilian carriers of a founder TP5

162 able increase in radiation-induced papillary thyroid carcinoma in children and young adults.

163 Here, we describe a novel model of thyroid carcinoma in zebrafish that reveals temporal cha

164 rtant for the development and progression of thyroid carcinomas in genetically permissive hosts.

165 ions known to date detects only a portion of thyroid carcinomas in preoperative FNAs in our cohort an

166 highly expressed in cell lines derived from thyroid carcinomas, in human thyroid carcinoma samples,

167 first 20 years there was a large increase in thyroid carcinoma incidence and a possible radiation-rel

168 We also assessed remission of medullary thyroid carcinoma, incidence and treatment of phaeochrom

169 of aggressive and refractory human advanced thyroid carcinomas, including local invasion and metasta

170 lecular signature of advanced and metastatic thyroid carcinoma involves deregulation of multiple fund

171 Medullary thyroid carcinoma is a relatively rare tumor with poor p

172 Anaplastic thyroid carcinoma is an aggressive malignancy that is al

173 tomy caused by local recurrence of papillary thyroid carcinoma is extremely rare.

174 Papillary thyroid carcinoma is frequently multifocal.

175 Interestingly, the prognosis of thyroid carcinoma is highly dependent on the age of the

176 adioiodine therapy (RITh) for differentiated thyroid carcinoma is performed either with thyroid hormo

177 Medullary thyroid carcinoma is the most common cause of death in p

178 Thyroid carcinoma is the most common endocrine malignanc

179 omic localization of recurrent or metastatic thyroid carcinoma, leading to improved diagnostic accura

180 differential pathway activation in papillary thyroid carcinomas, leading to different tumor phenotype

181 Thyroid carcinoma may be associated with the Brazilian f

182 er thyroidectomy for papillary or follicular thyroid carcinoma may be performed using diagnostic imag

183 Rb1(+/-)Nras(+/-) animals, distant medullary thyroid carcinoma metastases are associated with loss of

184 associated with the development of medullary thyroid carcinoma (MTC) and pathogenesis of multiple end

185 In patients with medullary thyroid carcinoma (MTC) and type 2A multiple endocrine n

186 Patients with hereditary medullary thyroid carcinoma (MTC) associated with multiple endocri

187 ivation of Ras or Raf in the human medullary thyroid carcinoma (MTC) cell line, TT, induces growth ar

188 All of the cases of medullary thyroid carcinoma (MTC) express the RET receptor tyrosin

189 Medullary thyroid carcinoma (MTC) is a neuroendocrine cancer that

190 Medullary thyroid carcinoma (MTC) is a neuroendocrine tumor mainly

191 Medullary thyroid carcinoma (MTC) is a rare endocrine tumor arisin

192 reatment of patients with advanced medullary thyroid carcinoma (MTC) is still a challenge.

193 g for Familial Colon Cancer Genes, Medullary Thyroid Carcinoma (MTC) Surveillance Study, Osteosarcoma

194 The prognosis of medullary thyroid carcinoma (MTC) varies from long- to short-term

195 thus preventing the development of medullary thyroid carcinoma (MTC), the dominant endocrinopathy in

196 therapy for patients with advanced medullary thyroid carcinoma (MTC).

197 ients with biochemical evidence of medullary thyroid carcinoma (MTC).

198 atients with distant metastasis of medullary thyroid carcinoma (MTC).

199 se 2 phenotypes is the presence of medullary thyroid carcinoma (MTC).

200 labeled with (111)In or (131)I in medullary thyroid carcinoma (MTC).

201 Medullary thyroid carcinomas (MTC), a tumor of the thyroid parafol

202 (pheochromocytomas) and malignant (medullary thyroid carcinomas, MTCs) tumors from patients with mult

203 lar thyroid adenoma (n = 10), and follicular thyroid carcinoma (n = 10) showed RASSF1A promoter hyper

204 of the two most common types of nonmedullary thyroid carcinoma, namely papillary thyroid carcinoma (P

205 in a large pedigree displaying non-medullary thyroid carcinoma (NMTC).

206 Sarcomas, breast and thyroid carcinomas occurred with similar frequency and l

207 oth solid tumors (osteosarcoma and papillary thyroid carcinoma) occurred in recipients of DRZ.

208 nic activation has long been demonstrated in thyroid carcinomas of follicular cell derivation, but no

209 cells were microinjected with the papillary thyroid carcinoma oncogene (RET/PTC1 short isoform, know

210 Arm B patients had other subtypes of thyroid carcinoma or prior chemotherapy, and did not req

211 To evaluate the characteristics of thyroid carcinoma over time, we carried out a retrospect

212 Papillary thyroid carcinoma overexpress transforming growth factor

213 redictors of poor survival in differentiated thyroid carcinomas (P =.027 and P =.007, respectively).

214 e well-defined foci of poorly differentiated thyroid carcinoma (PDTC).

215 RET mutation, and characterised by medullary thyroid carcinoma, phaeochromocytoma, and extra-endocrin

216 milies were cancer affected and, among them, thyroid carcinoma presented a prevalence of 10.9% (3 men

217 A substantial increase in papillary thyroid carcinoma (PTC) among children exposed to the ra

218 xamination of the mass confirmed a papillary thyroid carcinoma (PTC) and enlarged metastatic lymph no

219 edullary thyroid carcinoma, namely papillary thyroid carcinoma (PTC) and follicular thyroid carcinoma

220 ET/PTC3 (RP3) that is expressed in papillary thyroid carcinoma (PTC) and thyroid epithelia in Hashimo

221 that 63 of 110 (57%) human primary papillary thyroid carcinoma (PTC) cases expressed nuclear pY-STAT3

222 ollicular tumours resembling human papillary thyroid carcinoma (PTC) depending on the founder line ex

223 Papillary thyroid carcinoma (PTC) displays higher heritability tha

224 Papillary thyroid carcinoma (PTC) displays strong but so far large

225 Although papillary thyroid carcinoma (PTC) displays strong heritability, no

226 ients undergoing thyroidectomy for papillary thyroid carcinoma (PTC) have subclinical nodal disease a

227 Papillary thyroid carcinoma (PTC) is the most common histotype of

228 Papillary thyroid carcinoma (PTC) is the most common type of thyro

229 Biomarkers of papillary thyroid carcinoma (PTC) metastasis can accurately identi

230 A genome-wide association study of papillary thyroid carcinoma (PTC) pinpointed two independent SNPs

231 Papillary thyroid carcinoma (PTC) remained to be the most common t

232 mately 40 percent of patients with papillary thyroid carcinoma (PTC) typically have either intrachrom

233 he most common somatic mutation in papillary thyroid carcinoma (PTC), how it induces tumor aggressive

234 Papillary thyroid carcinoma (PTC), the most frequent thyroid cance

235 those associated with a precursor papillary thyroid carcinoma (PTC).

236 nts, which are frequently found in papillary thyroid carcinoma (PTC).

237 at exposure and risk of developing papillary thyroid carcinoma (PTC).

238 tle is known about the genetics of papillary thyroid carcinoma (PTC).

239 13) firmly associated with risk of papillary thyroid carcinoma (PTC).

240 e factors that were induced by RET/papillary thyroid carcinoma (PTC)3 gene expression including sever

241 Most papillary thyroid carcinomas (PTC) have an isozyme-specific reduct

242 g and expression analysis of eight papillary thyroid carcinomas (PTC) to comprehensively characterize

243 s detected in approximately 45% of papillary thyroid carcinomas (PTC).

244 most common genetic alteration in papillary thyroid carcinomas (PTC).

245 st prevalent genetic alteration in papillary thyroid carcinomas (PTC).

246 of genetic alterations detected in papillary thyroid carcinomas (PTC).

247 Papillary thyroid carcinomas (PTCs) account for 90% of human thyro

248 cation and treatment selection for papillary thyroid carcinomas (PTCs) do not uniformly predict tumor

249 Papillary thyroid carcinomas (PTCs) that invade into local structu

250 various thyroid neoplasms such as papillary thyroid carcinomas (PTCs), follicular thyroid adenomas a

251 oidectomies in China while other features of thyroid carcinoma remained similarly in the recent years

252 fforts, current knowledge of the etiology of thyroid carcinoma remains limited.

253 t common endocrine malignancy, and papillary thyroid carcinoma represents the most common thyroid can

254 ation of the RET proto-oncogene in papillary thyroid carcinomas results from rearrangements linking t

255 the rearranged during transfection/papillary thyroid carcinoma (RET/PTC) fusion oncogene family durin

256 es derived from thyroid carcinomas, in human thyroid carcinoma samples, and their metastases.

257 V/PV) mice) spontaneously develop follicular thyroid carcinoma similar to human cancer.

258 model that spontaneously develops follicular thyroid carcinoma similar to human thyroid cancer (Thrb(

259 se) that spontaneously develops a follicular thyroid carcinoma similar to human thyroid cancer.

260 /PV) mouse) spontaneously develop follicular thyroid carcinoma similar to human thyroid cancer.

261 or more SMNs, including four leukemias, five thyroid carcinomas, six breast carcinomas, and four sarc

262 to determine overall survival, and medullary thyroid carcinoma-specific survival based on whether the

263 Medullary thyroid carcinoma-specific survival curves did not show

264 lymorphism followed by DNA sequencing in 125 thyroid carcinoma specimens from 107 patients, to includ

265 possible role of ras genotyping to identify thyroid carcinoma subsets associated with poor prognosis

266 initiate distinct pathways of oncogenesis in thyroid carcinoma subtypes.

267 mas, and its expression pattern in medullary thyroid carcinomas suggested contribution of both hypoxi

268 noncoding RNA gene (lincRNA) named Papillary Thyroid Carcinoma Susceptibility Candidate 3 (PTCSC3) lo

269 testing group and 0.954 for patients in the thyroid carcinoma testing group.

270 th an AUC of 0.944 and 0.995 for the SCC and thyroid carcinoma testing groups, respectively.

271 Thyroid carcinomas that harbor RET/PTC oncogenes are wel

272 Papillary thyroid carcinomas that invade locally or metastasize ar

273 Combi-TA mice developed papillary thyroid carcinomas, the incidence of which was increased

274 correlated with the generation of papillary thyroid carcinomas, the most prevalent malignancy of the

275 tatic lesions of a mouse model of follicular thyroid carcinoma [thyroid hormone beta receptor (TRbeta

276 -AS was significantly downregulated in human thyroid carcinoma tissue specimens, particularly the ana

277 l trial to show responsiveness of anaplastic thyroid carcinoma to PD-1 blockade.

278 n insight into the pathogenesis of papillary thyroid carcinoma, transcriptional profiles of four norm

279 hyroid tumors of a mouse model of follicular thyroid carcinoma (TRbeta(PV/PV) mice).

280 arcinogenesis in a mouse model of follicular thyroid carcinoma (TRbetaPV/PV mouse).

281 ation of mutated RET gene in human medullary thyroid carcinoma TT cells.

282 We conclude that papillary thyroid carcinoma tumor cells exhibit increased cancer s

283 lder; total thyroidectomy for differentiated thyroid carcinoma; tumor-node-metastasis (TNM) stage, as

284 eatment of patients with well-differentiated thyroid carcinoma; usual amounts vary widely.

285 o underwent thyroidectomy for differentiated thyroid carcinoma was performed.

286 , follicular thyroid adenoma, and follicular thyroid carcinoma was quantified.

287 Among patients with differentiated thyroid carcinomas (WDC and PDC), 11 (55.0%) of 20 patie

288 st common other cancers in the patients with thyroid carcinoma were breast cancer (5 patients) and so

289 k thyroid tissues of patients with papillary thyroid carcinoma were quantified.

290 tatic solid tumors, patients with anaplastic thyroid carcinoma were treated with spartalizumab, a hum

291 ere associated with follicular and papillary thyroid carcinomas, whereas long telomeres and low level

292 We report a case of papillary thyroid carcinoma which invades IJV with hypervascular t

293 he tumour cells of a patient with follicular thyroid carcinoma, which affects the binding of the tumo

294 tation carriers have renal cell or papillary thyroid carcinomas, which are also CS-related features.

295 ged, they spontaneously developed follicular thyroid carcinoma with pathological progression from hyp

296 a novel CREB3L2-PPARgamma fusion mutation in thyroid carcinoma with t(3;7)(p25;q34), showing that a f

297 needs to be to achieve long-term control of thyroid carcinoma with tracheal invasion.

298 e redifferentiation in poorly differentiated thyroid carcinomas with constitutive activation of eithe

299 patients with metastatic, iodine-refractory thyroid carcinoma, with an overall clinical benefit rate

300 t also promotes the development of medullary thyroid carcinomas yielding metastases at a high frequen