ライフサイエンスコーパス: vascular invasion

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

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

3 helium of the developing CNS coincident with 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 hypertrophic chondrocyte layer and impaired vascular invasion.

9 apoptosis/mitosis ratio and uncommonly show vascular invasion.

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

11 e of hypertrophic chondrocytes with delay of vascular invasion.

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

13 was associated with T4 stage, N2 stage, and vascular invasion.

14 ascular invasion and 24.4% for patients with vascular invasion.

15 s associated with undifferentiated tumor and vascular invasion.

16 rrelates with tumor capsule breakthrough and vascular invasion.

17 in cancer cells that modulates motility and vascular invasion.

18 tumor cells to suppress HCC development and vascular invasion.

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

20 ge, pT stage, lymphatic invasion, and venous vascular invasion.

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

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

23 effect of DM on clinical outcomes including vascular invasion.

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

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

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

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

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

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

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

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

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

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

34 0 [95% CI, 3.34-8.11]; P < .001), extramural vascular invasion (76.9% vs 28.4%; relative risk, 2.71 [

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

36 nctioning and nodal status, tumor grade, and vascular invasion accurately predict survival and recurr

37 ow-up of patients with low-risk mPTC without vascular invasion after hemithyroidectomy.

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

39 e technique was unable to detect capsular or vascular invasion, although the specificity and positive

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

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

42 bability of RD was 1.3% for patients without vascular invasion and 24.4% for patients with vascular i

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

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

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

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

47 During vascular invasion and formation of ossification centers,

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

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

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

51 Vascular invasion and microscopic extrathyroidal extensi

52 Thus, vascular invasion and ossification start in the femoral

53 ficantly associated with lymphatic invasion, vascular invasion and perineural invasion, while CAP reg

54 ubdistribution regression, T-stage, N-stage, vascular invasion and positive margins were all predicti

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

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

57 This infection is characterized by vascular invasion and thrombosis.

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

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

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

61 , (2) promotes angiogenesis, (3) facilitates vascular invasion, and (4) preserves the structural inte

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

63 In the explant, 17.5% had vascular invasion, and 42.8% exceeded Milan criteria (un

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

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

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

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

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

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

70 pression were correlated with poor survival, vascular invasion, and larger tumor size.

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

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

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

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

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

76 e, depth of invasion, lymph node metastasis, vascular invasion, and pathological stage.

77 on was closely associated with tumor number, vascular invasion, and poor prognosis.

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

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

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

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

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

83 ses: multiple liver lesions, with or without vascular invasion" as an "M1a stage," is suggested.

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

85 at 2.46, N2 stage at 10.58, and presence of vascular invasion at 4.27.

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

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

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

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

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

91 Vascular invasion by tumor cells can be classified as gr

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

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

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

95 For vascular invasion detection, sensitivity of images obtai

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

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

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

99 Here we show that obstruction of vascular invasion during bone healing favours chondrogen

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

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

102 MR-derived extramural vascular invasion (EMVI) was found in 16.2% (n = 14), wi

103 halo sign, duct-penetrating sign, absence of vascular invasion, etc.).

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

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

106 splant, tumor diameter, tumor pathology, and vascular invasion, female sex was associated with a 25%

107 splant, tumor diameter, tumor pathology, and vascular invasion, female sex was associated with a 25%

108 n ten tumors, associated with increased peri-vascular invasion (Fisher's exact, p < 0.018).

109 n rate increased to 73% (p < 0.001), whereas vascular invasion gradually decreased to 20% in 2012-201

110 tioning tumors with no nodal involvement and vascular invasion had a negligible risk of recurrence at

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

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

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

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

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

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

117 The molecular drivers of vascular invasion in HCC are open for investigation.

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

119 cells in vitro, and inhibit the intracranial vascular invasion in mouse models.

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

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

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

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

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

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

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

127 Vascular invasion is associated with dismal prognosis an

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

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

130 he appearance of new extrahepatic lesions or vascular invasion lesions was associated with a worse ov

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

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

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

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

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

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

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

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

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

140 ed by a noninvasive imaging system to detect vascular invasion of dormant tumors and have used them t

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

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

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

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

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

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

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

148 No vascular invasion or cellular atypia were evident.

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

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

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

152 or unresectable intrahepatic tumours with no vascular invasion or metastasis to other organs.

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

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

155 5), more: lymphovascular invasion (OR 1.76), vascular invasion (OR 1.92), perineural invasion (OR 1.8

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

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

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

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

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

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

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

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

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

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

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

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

168 < 0.001), poor differentiation (P = 0.049), vascular invasion (P = 0.002), and outside Milan (P = 0.

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

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

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

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

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

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

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

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

177 Vascular invasion provides a direct route for tumor meta

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

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

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

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

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

183 Presence of vascular invasion together with embryonal carcinoma and

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

185 lations of CREB1 with tumor stage and grade, vascular invasion (V1) and lymphovascular invasion (L1)

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

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

188 Vascular invasion (VI) is a critical risk factor for HCC

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

190 fferentiation (PD), lymphatic invasion (LI), vascular invasion (VI), and perineural invasion (PN), wi

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

192 Acceleration of vascular invasion was also observed in transgene positiv

193 Vascular invasion was apparent at the time of bone forma

194 the appearance of new extrahepatic lesion or vascular invasion was associated with a poor prognosis.

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

196 On explant, vascular invasion was found in 23.7% of AC-DS versus 16.

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

198 ny Akt isoform reduced lung metastasis while vascular invasion was reduced with Akt1 or 3 loss.

199 Intratumoral vascular invasion was the only significant predictor of

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

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

202 ctioning tumors, tumor grade, N1 status, and vascular invasion were all independent predictors of rec

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

204 EBL and vascular invasion were independent predictors of OS and

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

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

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

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

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

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

211 Vascular invasion, which is the strongest predictor of d

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

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

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