ライフサイエンスコーパス: thyroid tumor

1 ode dissections contralateral to the largest thyroid tumor.

2 ed with the size and location of the primary thyroid tumor.

3 defining the TNM stage of such an aggressive thyroid tumor.

4 anaplasia and metastasis of ret/PTC1-induced thyroid tumors.

5 e for PTEN in the pathogenesis of follicular thyroid tumors.

6 ntly (78%) in FTC, the most malignant of the thyroid tumors.

7 rom normal tissue adjacent to the breast and thyroid tumors.

8 and in one of four families with breast and thyroid tumors.

9 tinguishing benign from malignant follicular thyroid tumors.

10 tragenic mutations of PTEN are infrequent in thyroid tumors.

11 enesis of familial and sporadic nonmedullary thyroid tumors.

12 to the TME of Braf(V600E)/Pten(-/-)/TPO-Cre thyroid tumors.

13 change, also displaying higher expression in thyroid tumors.

14 ct of mitochondrial one-carbon metabolism in thyroid tumors.

15 c-like and anaplastic features of follicular thyroid tumors.

16 induced thyroid tumors, but also in sporadic thyroid tumors.

17 n in mammals and ancestors to neuroendocrine thyroid tumors.

18 de, including bladder, melanoma, breast, and thyroid tumors.

19 -kappaB, similar to the expression levels in thyroid tumors.

20 d highly penetrant and poorly differentiated thyroid tumors.

21 in benign and well-differentiated malignant thyroid tumors.

22 6 protein is upregulated in human breast and thyroid tumors.

23 function and growth of malignant and benign thyroid tumors.

24 of heterozygosity, found in the majority of thyroid tumors.

25 ferent classes of benign and malignant human thyroid tumors.

26 mechanism and is up-regulated in many human thyroid tumors.

27 n thyroid cells and downregulated in primary thyroid tumors.

28 e development of pRB-deficient pituitary and thyroid tumors.

29 e in the initiation and progression of human thyroid tumors.

30 thyroid cancer is one of the most aggressive thyroid tumors.

31 ble to differentiate benign versus malignant thyroid tumors.

32 r carcinomas, present earlier than do benign thyroid tumors.

33 alignant thyroid lesions in 73 patients with thyroid tumors.

34 nd to be decreased or even absent in various thyroid tumors.

35 the technique to copy-number profiles in 10 thyroid tumors.

36 ter by sequencing bisulfite-treated DNA from thyroid tumors.

37 tumors, we conducted exome sequencing on 58 thyroid tumors (28 cancers, 30 benign nodules) from 19 p

38 PTEN expression in 139 sporadic nonmedullary thyroid tumors (55 FA, 27 follicular thyroid carcinomas,

39 f patients, our data document that malignant thyroid tumors after radiation exposure, including folli

40 Surgical extirpation of the thyroid tumor and cervical node metastases is the only p

41 ed approach through RNA-sequencing of paired thyroid tumor and non-tumor samples, we have identified

42 specimens, including 378 surgically resected thyroid tumors and 217 thyroid nodule FNA biopsy specime

43 thylation-specific PCR studies in 64 primary thyroid tumors and 6 thyroid cell lines.

44 study tests whether BRAF is also mutated in thyroid tumors and cell lines.

45 hyroid tumors, as compared with nononcocytic thyroid tumors and normal thyroid samples.

46 d with an increased risk of breast, skin and thyroid tumors and occasional cases of other cancers inc

47 ly showed that A-to-I editing is elevated in thyroid tumors and that ADAR1 is functionally important

48 We confirmed miR-200b overediting in thyroid tumors and we showed that edited miR-200b has we

49 e tumor suppressor miR-200b is overedited in thyroid tumors, and its levels of editing correlate with

50 ase inhibitor (CDKI) p27(Kip1) is present in thyroid tumors, and recent evidence demonstrates p27 dow

51 Follicular epithelial cell-derived thyroid tumors are common neoplasms comprised mainly of

52 Although most thyroid tumors are curable, some patients diagnosed with

53 Thyroid tumors arising from the follicular cells often h

54 igh copy transgenic mice developed bilateral thyroid tumors as early as 4 days of age.

55 racterize the lipid composition of oncocytic thyroid tumors, as compared with nononcocytic thyroid tu

56 netic polymorphism, Y609C, was seen in 7% of thyroid tumors but was not related to gene downregulatio

57 is elevated not only in human radio-induced thyroid tumors, but also in sporadic thyroid tumors.

58 ions in mitochondrial DNA occur in oncocytic thyroid tumors, but there is no information about their

59 n: A specific and selective visualization of thyroid tumor by targeting gal-3 was demonstrated in the

60 en 0 and 98% of transgenic progeny developed thyroid tumors by 10 months of age, indicating that tumo

61 s been made in the differential diagnosis of thyroid tumors by fine needle aspiration biopsy, specifi

62 unique genomic landscape of PHTS-associated thyroid tumors carries implications for molecular-target

63 Our data show that thyroid tumors carrying BRAF(V600E) mutations are exquis

64 s using mutant-allele-specific PCR and in 10 thyroid tumor cell lines by DNA sequencing of the PCR-am

65 We found that BRAF was mutated in 8 of 10 thyroid tumor cell lines, including 2 of 2 papillary car

66 In the thyroid tumor cell lines, MAX loss triggers a marked shi

67 gger apoptosis in vitro in several resistant thyroid tumor cell lines, such as thyroid anaplastic car

68 In human thyroid tumor cell lines, we observed that TSHR was norm

69 on exhibited strong promoter activity in two thyroid tumor cell lines.

70 A methylation with BRAF mutation was seen in thyroid tumor cell lines.

71 luciferase expression in both SL-2 cells and thyroid tumor cell lines.

72 ed proliferation, invasion, and migration in thyroid tumor cell models.

73 Physiologically, ESRRA depletion suppressed thyroid tumor cell survival via caspase-dependent apopto

74 s of oncocytic or ESRRA-overexpressing human thyroid tumor cells in mice.

75 reased incorporation of bromodeoxyuridine in thyroid tumor cells of Thrb(PV/PV)-PTU mice, indicative

76 Overexpression of NCoR in thyroid tumor cells of TRbetaPV/PV mouse reduced PI3K si

77 R protein levels were significantly lower in thyroid tumor cells than in wild-type thyrocytes, allowi

78 eased mortalin expression only in follicular thyroid tumor cells.

79 At that time, clinical decisions regarding thyroid tumor classification were made by our multidisci

80 The thyroid tumors closely phenocopied the histological feat

81 showed 136% 88 greater uptake in orthotopic thyroid tumors compared with pulmonary lesions, which re

82 wed 136% +/- 88 greater uptake in orthotopic thyroid tumors compared with pulmonary lesions, which re

83 Results TAM levels were higher in orthotopic thyroid tumors compared with pulmonary metastatic lesion

84 Results TAM levels were higher in orthotopic thyroid tumors compared with pulmonary metastatic lesion

85 idly growing and strikingly large multilobed thyroid tumors containing mixtures of both well and poor

86 The ability to identify invasive follicular thyroid tumors could avert over 14,000 thyroidectomies a

87 Characterizing the genomic landscape in PHTS thyroid tumors could provide insights into malignant pot

88 ot affect growth of normal or non-anaplastic thyroid tumor cultures (differentiated carcinoma, benign

89 PHTS-associated thyroid tumors demonstrated a high frequency of second-h

90 ession was extinguished in a subset of human thyroid tumor-derived cell lines.

91 ify events that cooperate with Hras(G12V) in thyroid tumor development.

92 Thyroid tumors did not metastasize in any of the experim

93 clude tumors covering the entire spectrum of thyroid tumor differentiation.

94 We used CGH to study 33 thyroid-tumor DNAs and two tumor-cell-line DNAs.

95 Importantly, we detected both pituitary and thyroid tumors earlier in the Rb+/-p27-/- mice.

96 Multiple thyroid tumor foci from 10 of 17 patients yielded DNA of

97 The risk of benign thyroid tumors following such radiation exposure is much

98 Aggressive thyroid tumors (for example, anaplastic or poorly differ

99 oid-targeted expression of RET/PTC1 leads to thyroid tumor formation in Tg-PTC1 transgenic mice.

100 these signaling pathways in RET/PTC1-induced thyroid tumor formation in vivo, we generated and charac

101 Thyroid tumors found in this population were reviewed wi

102 le was lost from renal, uterine, breast, and thyroid tumors from a single patient.

103 We found that thyroid tumor growth was reduced by approximately 42% in

104 significantly increased survival, decreased thyroid tumor growth, delayed tumor progression and lowe

105 nables high penetrance of pituitary, but not thyroid, tumor growth in triple mutant animals (88% of R

106 PHTS-associated thyroid tumors had a unique genomic landscape in the set

107 A subset of thyroid tumors have loss of heterozygosity of chromosome

108 We conclude that a subset of thyroid tumors have somatic deletions of the PTEN gene,

109 or allele G and major allele T) in PIK3CA in thyroid tumors in 503 subjects by PCR and sequencing of

110 ncy significantly decreased the incidence of thyroid tumors in Pten(+/-), which correlates with the r

111 We analysed 42 differentiated thyroid tumors including 15 follicular adenomas (FA), 13

112 Treatment of orthotopic thyroid tumors, initiated 1 week after tumor cell implan

113 TC will provide an excellent system to study thyroid tumor initiation and progression and the evaluat

114 rthermore, transplantation of RP3-expressing thyroid tumors into naive mice resulted in leukocytic in

115 The type and molecular pathology of the thyroid tumors is changing with increasing latency, long

116 e that a molecular classification system for thyroid tumors is possible, and this in turn may provide

117 been found in benign and malignant sporadic thyroid tumors, loss of heterozygosity (LOH) has been re

118 Conditional Rb ablation resulted in thyroid tumors mimicking human MTC, and additional p53 l

119 We further tested this effect on a mouse thyroid tumor model, when in vivo tumor growth was also

120 iagnostic study analyzed surgically resected thyroid tumors obtained from February 2016 to April 2022

121 Thyroid tumors occurred at a median of 9.9 (4.5-22.3) ye

122 We found elevated PTTG1 levels in the thyroid tumors of a mouse model of follicular thyroid ca

123 role in oncogenesis, was highly elevated in thyroid tumors of TRbeta(PV/PV) mice.

124 Immunohistochemical analysis of 141 thyroid tumors of various histological types showed sign

125 We studied 95 sporadic thyroid tumors, of which 39 were papillary thyroid carci

126 firming it to be a germline genetic event in thyroid tumor patients.

127 system may be used to study genes modifying thyroid tumor penetrance in the dominantly inherited hum

128 function events that significantly increased thyroid tumor penetrance in Tpo-Cre/homozygous FR-Hras(G

129 these two epigenetic/genetic alterations in thyroid tumor progression, we examined their occurrences

130 tigation into the role inflammation plays in thyroid tumor progression.

131 f PI3K signaling and could serve to modulate thyroid tumor progression.

132 Here we show that in thyroid tumors, PV mutant bound significantly more to th

133 the frequent mutational activation of Ras in thyroid tumors reflects the ability of Ras-expressing ce

134 Sensitive VAF assays of 378 thyroid tumors revealed the presence of the BRAF V600E v

135 Diagnostic CL were imaged in a human thyroid tumor sample with reduced interference of isobar

136 In this study, we analyzed 197 thyroid tumor samples and showed that Rap1GAP was freque

137 udy we assess beta-catenin alteration in 145 thyroid tumors samples from 127 patients.

138 Immunohistochemical analysis of 142 thyroid tumors showed a statistically significant reduct

139 icating that SOD3 might be a novel player in thyroid tumor stroma.

140 -) mice grew more (and larger) pituitary and thyroid tumors than Rb1(+/-) mice.

141 murine model of BRAFV600E-induced PTC led to thyroid tumors that were more proliferative and larger t

142 contributes to the pathogenesis of papillary thyroid tumor, the time of tumor onset and the early phe

143 Ras mutations are frequent in thyroid tumors, the most common endocrine malignancy.

144 In thyroid tumors, three possibly inhibitory splice variant

145 ongly down-regulated (P = 2.84 x 10(-14)) in thyroid tumor tissue of 46 PTC patients and the risk all

146 A total of 438 surgically resected thyroid tumor tissues and 249 thyroid nodule FNA biopsie

147 This SNP was found in both normal and thyroid tumor tissues as well as in different generation

148 analyzed BRAF gene mutation at codon 599 in thyroid tumors using mutant-allele-specific PCR and in 1

149 l the somatic alterations in PHTS-associated thyroid tumors, we conducted exome sequencing on 58 thyr

150 In all, 38 sporadic thyroid tumors were analyzed.

151 Telomere lengths of 61 thyroid tumors were examined by fluorescence in situ hyb

152 d carcinoma is a distinct class of malignant thyroid tumor with a group of distinct genetic alteratio

153 analyzed a cohort of 378 surgically resected thyroid tumors with a maximum dimension of 1 cm or large

154 tient differences in RAS variants present in thyroid tumors with a variety of histopathological diagn

155 y distinguishes between benign and malignant thyroid tumors with excellent sensitivity and specificit

156 tumor suppressor gene develop pituitary and thyroid tumors with high penetrance.

157 ression and activity were relatively high in thyroid tumors with oncocytic characteristics, wherein E