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

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

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

7 tinguishing benign from malignant follicular thyroid tumors.

8 tragenic mutations of PTEN are infrequent in thyroid tumors.

9 enesis of familial and sporadic nonmedullary thyroid tumors.

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

11 n in mammals and ancestors to neuroendocrine thyroid tumors.

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

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

14 d highly penetrant and poorly differentiated thyroid tumors.

15 in benign and well-differentiated malignant thyroid tumors.

16 6 protein is upregulated in human breast and thyroid tumors.

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

18 ferent classes of benign and malignant human thyroid tumors.

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

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

21 n thyroid cells and downregulated in primary thyroid tumors.

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

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

24 ble to differentiate benign versus malignant thyroid tumors.

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

26 alignant thyroid lesions in 73 patients with thyroid tumors.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

41 Thyroid tumors arising from the follicular cells often h

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

61 The thyroid tumors closely phenocopied the histological feat

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

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

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

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

66 Thyroid tumors did not metastasize in any of the experim

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

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

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

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

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

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

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

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

75 Thyroid tumors found in this population were reviewed wi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

115 In thyroid tumors, three possibly inhibitory splice variant

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

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

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

119 In all, 38 sporadic thyroid tumors were analyzed.

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

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

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