ライフサイエンスコーパス: vascular invasion

1 metastasis, extrahepatic extension, or major vascular invasion).

2 hypertrophic chondrocyte layer and impaired vascular invasion.

3 in cancer cells that modulates motility and vascular invasion.

4 nvasive carcinoma, positive lymph nodes, and vascular invasion.

5 vasive component, lymph node metastases, and vascular invasion.

6 ulti-detector row CT most accurately display vascular invasion.

7 face of endothelial cells, thereby promoting vascular invasion.

8 apoptosis/mitosis ratio and uncommonly show vascular invasion.

9 , carcinoma in situ, and gastric cancer with vascular invasion.

10 e of hypertrophic chondrocytes with delay of vascular invasion.

11 r tumor stage, tumor grade, and suspicion of vascular invasion.

12 tumor cells to suppress HCC development and vascular invasion.

13 targeting of TET1, thereby leading to tumor vascular invasion.

14 multiple tumors, lymph node metastasis, and vascular invasion.

15 tial resection margin; and E, for Extramural vascular invasion.

16 effect of DM on clinical outcomes including vascular invasion.

17 pha-fetoprotein more than 100 ng/mL, and any vascular invasion.

18 rrelates with tumor capsule breakthrough and vascular invasion.

19 mor thickness, more spitzoid tumors and more vascular invasion.

20 Spitzoid histology, radial growth phase, and vascular invasion.

21 clude that Notch signaling is crucial for TB vascular invasion.

22 , positive resection margin, perineural, and vascular invasion.

23 of grade, tumor type, nodal metastases, and vascular invasion.

24 helium of the developing CNS coincident with vascular invasion.

25 2), lymph node metastasis (2.09; 1.80-2.43), vascular invasion (1.87; 1.44-2.42), and poor tumor diff

26 logy (55), extracapsular extension (107), or vascular invasion (119).

27 Of 608 patients beyond Milan without vascular invasion, 480 (79%) patients underwent resectio

28 ifferentiation (44% vs. 26%, P < 0.001); (4) vascular invasion (54% vs. 33%, P < 0.001); (5) perineur

29 t patients had a solitary tumor (73%) and no vascular invasion (69%).

30 0 [95% CI, 3.34-8.11]; P < .001), extramural vascular invasion (76.9% vs 28.4%; relative risk, 2.71 [

31 s were solitary (74%) and had no evidence of vascular invasion (82%).

32 rrence were albumin less than 3.5 gm/dL, any vascular invasion, age more than 60 years, tumor size la

33 ssion from hyperplasia to capsular invasion, vascular invasion, anaplasia and metastasis to the lung,

34 ogression of hyperplasia, capsular invasion, vascular invasion, anaplasia, and eventually, distant or

35 f cHCC, the former had a higher incidence of vascular invasion and a poorer long-term survival.

36 n hepatocellular carcinoma (HCC) tumors with vascular invasion and can promote HCC cell invasiveness

37 Norrin production leads to premature retinal vascular invasion and delayed Norrin production leads to

38 edicted tumor recurrence and correlated with vascular invasion and differentiation.

39 During vascular invasion and formation of ossification centers,

40 bone formation, Lbh may negatively regulate vascular invasion and formation of the early ossificatio

41 s, significantly increased the occurrence of vascular invasion and lung metastasis.

42 n also mainly contributes to the blockage of vascular invasion and metastasis of HCC.

43 Thus, vascular invasion and ossification start in the femoral

44 nimal studies, aggressive biologic behavior (vascular invasion and recurrence) correlates significant

45 Runx2(-/-)/PTHrP(-/-) mice exhibited limited vascular invasion and some chondrocytes expressing colla

46 This infection is characterized by vascular invasion and thrombosis.

47 ons required to inhibit MMPs in vitro and in vascular invasion and tumor proliferation in vivo models

48 Those with symptoms of HCC and/or vascular invasion and/or extrahepatic cancer are conside

49 ber of nodules, and presence of intrahepatic vascular invasion), and presence of extrahepatic vascula

50 mance status (PS) >/=1, 41% with macroscopic vascular invasion, and 38% with extrahepatic tumor sprea

51 rs exceeding the Milan criteria, macroscopic vascular invasion, and AFP score>2 were independent pred

52 rade, tumor size, lymph node involvement and vascular invasion, and biomarkers (eg, estrogen receptor

53 oorer residual liver function, more frequent vascular invasion, and diabetes mellitus were also obser

54 athologic determinants follicular histology, vascular invasion, and extracapsular extension.

55 radiologist who evaluated presence of tumor, vascular invasion, and flow artifacts in the superior me

56 ted in loss of columnar structure, premature vascular invasion, and formation of ectopic hypertrophic

57 des no prognostic information, tumor number, vascular invasion, and LN metastasis were associated wit

58 tem for ICC that focuses on multiple tumors, vascular invasion, and lymph node metastasis.

59 ickness; and presence of biliary dilatation, vascular invasion, and lymphadenopathy were assessed.

60 he prevalence of nodal metastases, lymphatic vascular invasion, and multifocal neoplasia in patients

61 istics of the tumors, including growth rate, vascular invasion, and p53 overexpression.

62 ed implants readily underwent calcification, vascular invasion, and subsequent endochondral ossificat

63 n histoscores correlated with poor outcomes, vascular invasion, and time to recurrence.

64 ade, tumour size, oestrogen-receptor status, vascular invasion, and treatment assignment (hazard rati

65 The time to development of metastases, vascular invasion, and/or new lesions was 13.8 months (c

66 bar tumor distribution, tumor size, grade of vascular invasion, artificial neural network models pred

67 es of the primary tumor (i.e., stage, grade, vascular invasion) assist in identifying patients who wo

68 iology score; cancer stage; differentiation; vascular invasion; blood transfusion; and postoperative

69 Thus, PTHrP must slow vascular invasion by a mechanism independent of the PTH/

70 ted with malignant features such as areas of vascular invasion by hepatocytes and heterogeneous hyper

71 indings can be used to predict perineural or vascular invasion by oral cavity tumors.

72 rence screen was used to identify drivers of vascular invasion by panning small hairpin RNA (shRNA) l

73 Vascular invasion by tumor cells can be classified as gr

74 istopathologic findings of perineural and/or vascular invasion by tumor were correlated in all patien

75 cm grade 2 invasive cancer without lymphatic vascular invasion; clean margins were obtained, and both

76 or size larger than 7 cm and the presence of vascular invasion correlated significantly with recurren

77 For vascular invasion detection, sensitivity of images obtai

78 ouble-homozygous knockout mice, the delay in vascular invasion did not occur.

79 pathologic stage, nuclear grade, microscopic vascular invasion, DNA content, nuclear morphometry, and

80 gest that activated MMP2 does not facilitate vascular invasion during angiogenesis unless it forms a

81 metastatic potential, tumor grade, and lymph-vascular invasion during breast cancer progression.

82 atients with N1 disease, multiple tumors and vascular invasion, either alone or together, failed to d

83 L on multivariate analysis were male gender, vascular invasion, extent of hepatectomy, and operative

84 nodules, intra- and extrahepatic macroscopic vascular invasion, extrahepatic metastases).

85 ria, CT findings predictive of perineural or vascular invasion had a sensitivity of 88%; specificity,

86 Microscopic vascular invasion (hazard ratio = 3.40, 95% confidence i

87 to recurrence beyond MC included microscopic vascular invasion (hazard ratio [HR] 2.38 [range, 1.10-7

88 , multiple lesions (HR, 1.80; P = .001), and vascular invasion (HR, 1.59; P = .015).

89 R]: 1.51), multifocal tumors (HR: 1.51), and vascular invasion (HR: 1.44) remained independent predic

90 rometastases correlated with the presence of vascular invasion in both protocols.

91 creased KLF6 mRNA levels and the presence of vascular invasion in human HCC.

92 ansgene restored chondrocyte hypertrophy and vascular invasion in the bones of the mutant mice but di

93 isk or low-risk of recurrence by presence of vascular invasion in the surgical specimen.

94 est a relationship between higher BMI, tumor vascular invasion, increased recurrence, and worsened ov

95 ALN also inhibited vascular invasion into the calcified cartilage in rats w

96 y mechanical loading significantly inhibited vascular invasion into the defect by 66% and reduced bon

97 ascular plexus, the outer plexus, and deeper vascular invasion into the outer and subretinal spaces w

98 Cancer cell vascular invasion is a crucial step in the malignant pro

99 Vascular invasion is associated with dismal prognosis an

100 ng-standing systems biology conundrum of how vascular invasion is coordinated with tissue development

101 RNA (miRNA) expression plays a role in tumor vascular invasion is unclear.

102 left kidney diagnosed as clear cell RCC with vascular invasion, liver, lung and brain metastasis.

103 In an in vitro model of vascular invasion, loss of ADAM15 reduced PC-3 adhesion

104 ford modified Gleason scale), cancer volume, vascular invasion, lymph node involvement, seminal vesic

105 f tumor nodules, size of the largest nodule, vascular invasion, metastasis, serum albumin, and alpha-

106 re able to be stratified by tumor number and vascular invasion (N0; P < .001), among patients with N1

107 survival (DSS) of tumor size, mitotic rate, vascular invasion, necrosis, metastases, and nuclear gra

108 enhancement/size, development/progression of vascular invasion, new hepatic lesions) progression or (

109 race, tumor grade, stage at diagnosis, lymph/vascular invasion, number of primary tumors, tumor size,

110 ce was also observed in a zebrafish model of vascular invasion of cancer cells after injection into t

111 rsors, labeled in the perichondrium prior to vascular invasion of the cartilage, give rise to trabecu

112 cruitment and migration are required for the vascular invasion of the cartilaginous anlage and the os

113 tion in the primary spongiosa and a delay in vascular invasion of the early cartilage model.

114 We demonstrate that MMP9 mediates vascular invasion of the hypertrophic cartilage callus,

115 relate with grade or presence of microscopic vascular invasion on final pathology.

116 nced the relative effect of tumor number and vascular invasion on prognosis.

117 Adenopathy (two patients) and vascular invasion (one patient) were not identified radi

118 Runx2(-/-) femurs exhibited no vascular invasion or chondrocytes expressing collagen ty

119 y Group performance score (ECOG PS; 0 or 1), vascular invasion or extrahepatic spread (yes or no), an

120 Asian, 66.6%; ECOG PS 0, 65.2%; HBV, 49.1%; vascular invasion or extrahepatic spread, 70.1%).

121 and who had solitary HCC up to 3 cm without vascular invasion or metastasis was retrospectively iden

122 ular invasion), and presence of extrahepatic vascular invasion or metastasis were included, and rando

123 l plexus were secondary to retinal thinning, vascular invasion, or a combination of both.

124 oid cancer (containing follicular histology, vascular invasion, or extracapsular extension) showed no

125 ogesterone receptor expression, tumor stage, vascular invasion, or proliferation index.

126 s most adversely affected by the presence of vascular invasion (P < .05).

127 Diffuse type (P < 0.001), macro vascular invasion (P < 0.001) and late stage tumours (P

128 Female gender (P < 0.05), vascular invasion (P < 0.001), tumours over 5 cm (P < 0.

129 Independent predictors of death were major vascular invasion (P <.001), microvascular invasion (P =

130 ors, any more than 5 cm, or tumor with major vascular invasion (P <.001).

131 atures such as perineural, lymphatic, and/or vascular invasion (P = .0004).

132 Only vascular invasion (P = .001) and CES-D score > or = 16 (

133 ent (P < .0001), tumor type (P < .0001), and vascular invasion (P = .0077) all showed statistically s

134 , tumor size greater than 5 cm (p = 0.0221), vascular invasion (p = 0.0005), positive nodes (p = 0.00

135 < 0.001), poor differentiation (P = 0.049), vascular invasion (P = 0.002), and outside Milan (P = 0.

136 PPAR gamma rearrangement more frequently had vascular invasion (P = 0.01), areas of solid/nested tumo

137 alpha-fetoprotein >200 ng/mL (P = 0.04), and vascular invasion (P = 0.017) as significant predictors

138 se RFS, grade 4 HCC's (P < 0.0001, HR: 5.6), vascular invasion (P = 0.019, HR: 2.0), size >3 cm (P <

139 per 50 high-power fields (P =.001, P =.002), vascular invasion (P =.02, P =.04), size < or = 2 cm (P

140 olvement matched that of patients with major vascular invasion (P =.3).

141 t allocation is based on tumor number, size, vascular invasion, performance status, functional liver

142 r grade, nodal metastases, resection margin, vascular invasion, perineural invasion, p53 or Smad4 lev

143 Tumor-related factors such as vascular invasion primarily determine long-term outcomes

144 Vascular invasion provides a direct route for tumor meta

145 howed significant correlation with increased vascular invasion rate and microvessel density as well a

146 Ki-67, S-phase fraction, mitotic index, and vascular invasion showed a significant association with

147 Ki-67, S-phase fraction, mitotic index, and vascular invasion showed a significant association with

148 histologic grade, tumor type, invasive size, vascular invasion status, and lymph node status.

149 wing for tumour size, lymph-node status, and vascular invasion, the effect of micrometastases decreas

150 Presence of vascular invasion together with embryonal carcinoma and

151 ied model of stratification that is based on vascular invasion, tumor number, and tumor size and inco

152 ctal dilatation, local invasion, adenopathy, vascular invasion, vascular encasement, metastases, and

153 ients with HCC who had pathologically proven vascular invasion (VI) because of the associated increas

154 Vascular invasion (VI) was present in 17% of tumors and

155 plete capsular invasion (Ci), or both but no vascular invasion (Vi).

156 Acceleration of vascular invasion was also observed in transgene positiv

157 Vascular invasion was apparent at the time of bone forma

158 head of the pancreas, metastatic disease or vascular invasion was discovered frequently by laparosco

159 Histological vascular invasion was present in 18 (62%) patients, and

160 Intratumoral vascular invasion was the only significant predictor of

161 grade predicted the presence of microscopic vascular invasion (well, 15.7%; moderate; 31.9%, poor; 5

162 CT criteria for diagnosis of perineural or vascular invasion were aggressive tumor margins, invasio

163 an alpha-fetoprotein level >2000 ng/ml, and vascular invasion were also determinants of poor outcome

164 EBL and vascular invasion were independent predictors of OS and

165 tive lymph node findings, and intraprostatic vascular invasion were independently associated with pro

166 or satellites close to the primary tumor and vascular invasion were observed, indicating early invasi

167 itive lymph node findings and intraprostatic vascular invasion were the only other variables that rem

168 e I NSGCC, including high-risk patients with vascular invasion, were observed in a surveillance progr

169 r size greater than 5 cm and the presence of vascular invasion (which confirm several, single-center

170 ole in growth plate maturation by regulating vascular invasion, which is crucial for replacement of t

171 Vascular invasion, which is the strongest predictor of d

172 Ossification is preceded by vascular invasion, which occurs along rows of enthesis f

173 rentiation, low apoptosis/mitosis ratio, and vascular invasion) while still small, similar to flat ca

174 d no nodal involvement, metastases, or major vascular invasion) who underwent surgical resection (not