ライフサイエンスコーパス: lymphovascular

1 1 (91%); mesoappendix involvement 3 mm (5%); lymphovascular (15%) or perineural (24%) invasion; and p

2 uently changed elements were grade (40%) and lymphovascular (26%), nodal (15%), and margin (12%) stat

3 This organ-specific lymphovascular abnormality can be rescued by allowing em

4 Tumor size (best cut-off at 1.95 cm), lymphovascular and perineural invasion, and pT classific

5 iewed for the presence and the number of TD, lymphovascular and perineural invasion.

6 grade of differentiation, mucinous subtype, lymphovascular, and perineural invasion.

7 Spheroidgenesis and lymphovascular emboli formation are the direct result of

8 BC xenograft, MARY-X, which manifests florid lymphovascular emboli in severe combined immunodeficient

9 This model exhibited lymphovascular emboli in vivo and corresponding spheroid

10 alence of xenograft-generated spheroids with lymphovascular emboli in vivo with both structures demon

11 This Notch 3 addiction of lymphovascular emboli might be exploited in future thera

12 xhibited by MARY-X also was exhibited by the lymphovascular emboli of human IBC cases independent of

13 The lymphovascular emboli of human IBC exhibited dual N3icd

14 jected i.v. immunolocalized to the pulmonary lymphovascular emboli of MARY-X and caused their dissolu

15 ere only weakly tumorigenic and did not form lymphovascular emboli.

16 ysis of E-cad generates the formation of the lymphovascular embolus and is responsible for its unique

17 adherin overexpression in the genesis of the lymphovascular embolus of IBC.

18 However, within the lymphovascular embolus, E-cad and its proteolytic proces

19 Grading G2 [odds ratio (OR) 6.04], lymphovascular infiltration (OR 10.17), size (OR 18.50),

20 multivariate analysis, grading G2 (OR 6.98), lymphovascular infiltration (OR 8.63), and size >15.5 mm

21 r size >15.5 mm, grading G2, and presence of lymphovascular infiltration are factors independently re

22 dex, localization, mesoappendiceal invasion, lymphovascular infiltration).

23 , tumour depth (T1bsm2-3 17.6% vs T1a 7.1%), lymphovascular invasion (17.2% vs 12.6%), or signet cell

24 Clusters 2, 3, and 4 were associated with lymphovascular invasion (19 of 50 [38%], 14 of 34 [41%],

25 t nodal metastasis had a higher frequency of lymphovascular invasion (26.3% vs 8.1%; P < .001), perin

26 on frozen section (62% v 8%, P < .001), have lymphovascular invasion (38% v 24%, P < .001), and recei

27 A-IPMN patients had lower T-stage, lymphovascular invasion (51.4% vs. 75.6%), perineural in

28 rade carcinoma (66.7 vs 1.4%, p < 0.001) and lymphovascular invasion (77.8 vs 44.4%, p = 0.011) than

29 39, 4: OR 4.15, X: OR 1.87), and presence of lymphovascular invasion (absent: reference, present: OR

30 entiated tumors, right-sided laterality, and lymphovascular invasion (all p < 0.0001).

31 nical node-positive disease (ASD, 0.40), and lymphovascular invasion (ASD, 0.25).

32 ties (hazard ratio, 6.20; 95% CI, 1.4-27.7), lymphovascular invasion (hazard ratio, 4.7; 95% CI, 1.0-

33 [hazard ratio (HR) = 1.8; 95% CI, 1.2-2.8], lymphovascular invasion (HR = 2.2; 95% CI, 1.4-3.4), and

34 7), R1 vs R0 (HR, 5.21; 95% CI, 2.58-10.54), lymphovascular invasion (HR, 4.47; 95% CI, 1.43-13.99),

35 o test the significance of adding grade (G), lymphovascular invasion (L), estrogen receptor (ER) stat

36 stage and grade, vascular invasion (V1) and lymphovascular invasion (L1) were found.

37 that bladder cancer patients with associated lymphovascular invasion (LVI) are at increased risk of o

38 endometrioid adenocarcinoma with 80% MMI and lymphovascular invasion (LVI) involving the outer half o

39 Lymphovascular invasion (LVI) was the only clinicopathol

40 p53 protein expression and lymphovascular invasion (LVI) were evaluated for predict

41 in situ (DCIS), invasive carcinoma (IC), or lymphovascular invasion (LVI), and 8% lobular neoplasia

42 status, histologic tumor grade, presence of lymphovascular invasion (LVI), and receipt of chemothera

43 ow thickness, mitotic rate (MR), ulceration, lymphovascular invasion (LVI), and regression; incidence

44 26 (IQR, 19-34); perineural invasion (PNI), lymphovascular invasion (LVI), and residual positive mar

45 SBE] and long segment [LSBE]), nodal status, lymphovascular invasion (LVI), and the presence of multi

46 adverse prognostic factors are younger age, lymphovascular invasion (LVI), high Ki-67, and larger tu

47 eceptor status, HER2/neu status, presence of lymphovascular invasion (LVI), number of SLN(s) identifi

48 cinoma (IBC) is characterized by exaggerated lymphovascular invasion (LVI), recapitulated in our huma

49 , grade, positive margin, nodal involvement, lymphovascular invasion (LVI), stage, lymph node ratio,

50 r emboli within lymphovascular spaces termed lymphovascular invasion (LVI).

51 eals a 1.5 cm IDC that is high grade without lymphovascular invasion (LVI).

52 and significantly higher in the presence of lymphovascular invasion (LVI; 0.25 +/- 0.02 v 0.17 +/- 0

53 differentiation grade (OR 1.66), microscopic lymphovascular invasion (OR 1.70), a lymph node ratio >

54 subclassification (OR 2.56/1.59/1.75), more: lymphovascular invasion (OR 1.76), vascular invasion (OR

55 [95% CI, 1.22-1.48]; P < .001), presence of lymphovascular invasion (OR, 1.26 [1.19-1.33]; P < .001)

56 nodal metastasis (OR, 3.400; P = 0.017) and lymphovascular invasion (OR, 3.055; P = 0.045).

57 or higher (OR, 3.70; 95% CI, 1.4-10.0), and lymphovascular invasion (OR, 3.84; 95% CI, 2.1-6.9).

58 ted with grade 3 tumors (P = .0007) and with lymphovascular invasion (P < .0001).

59 ated with poor differentiation (P = 0.0015), lymphovascular invasion (P < 0.0001), and tumor size >/=

60 merican Joint Committee on Cancer stage, and lymphovascular invasion (P < 0.0001, P < 0.0001, P = 0.0

61 alysis showed that tumor number (P < 0.001), lymphovascular invasion (P < 0.001), and poor differenti

62 Lymph node metastases (P < 0.001), lymphovascular invasion (P < 0.001), and the presence of

63 perineural invasion (P = 0.023), as well as lymphovascular invasion (P = 0.005) in PDAC.

64 reslow thickness (P = 0.012) and presence of lymphovascular invasion (P = 0.018) were the only factor

65 of nuclear expression of DDIT4 protein, and lymphovascular invasion (P = 0.025), as well as advanced

66 rentiated tumors (P = 0.004) and presence of lymphovascular invasion (P = 0.031).

67 ciated with high tumor grade (P = 0.015) and lymphovascular invasion (P = 0.048).

68 nt (P<.001), infiltrative growth (P=.01), or lymphovascular invasion (P=.01).

69 The presence of lymphovascular invasion and clinically, but not microsco

70 -dimer, is a clinically important marker for lymphovascular invasion and early tumor metastasis in op

71 ll-differentiated invasive carcinoma without lymphovascular invasion and intermediate grade ductal ca

72 d it was an independent predictive marker of lymphovascular invasion and lymph node involvement.

73 sion was associated with muscle, neural, and lymphovascular invasion and the presence and number of i

74 with a greater percentage of recurrence and lymphovascular invasion and with lower disease-free surv

75 ivariate analysis, pathologic response >95%, lymphovascular invasion and/or perineural invasion (PNI)

76 r receptor 2 (HER2) status, tumor grade, and lymphovascular invasion are relevant; Oncotype DX score

77 Typically, it presents with lymphovascular invasion as well as metastasis at the tim

78 oup, clinical stage, residual mass size, and lymphovascular invasion at orchiectomy, the presence of

79 The step of intravasation or lymphovascular invasion can be a rate-limiting step in t

80 I tumors, although markers such as grade and lymphovascular invasion did not add value in this subset

81 Importantly, only 1 of 132 patients without lymphovascular invasion died of MCC.

82 might shed light on the general mechanism of lymphovascular invasion exhibited by all metastasizing c

83 ed patients, more patients with than without lymphovascular invasion had detectable TTMV HPV DNA (12

84 carcinoma manifests an exaggerated degree of lymphovascular invasion in situ; hence, a study of its m

85 Lymphovascular invasion in the orchiectomy specimen, a h

86 ted D-dimer levels predicted the presence of lymphovascular invasion in univariate logistic regressio

87 is cohort, especially among patients showing lymphovascular invasion on biopsy.

88 ents with T2-3, N0 rectal cancers and either lymphovascular invasion or elevated CEA levels have redu

89 e of tumours, patient age, histologic grade, lymphovascular invasion or perineural invasion positivit

90 High-risk (lymphovascular invasion positive) patients with CS1 NSGC

91 gative, PgR-negative, HER2-negative) tumors, lymphovascular invasion positivity, or estimated distant

92 sis (2 factors: HR, 4.1 [95% CI, 1.0-16.6]), lymphovascular invasion predicted death from disease (HR

93 ent age, tumor size, palpability, grade, and lymphovascular invasion predicted lymph node status.

94 gher CA19-9 levels as well as perineural and lymphovascular invasion rates compared to the lung oligo

95 riate analysis, patient age, tumor size, and lymphovascular invasion remained significant.

96 Lymphovascular invasion was present.

97 Lymphovascular invasion was the only significant factor

98 Pathologic stage and lymphovascular invasion were independent predictors of D

99 easing Clark level, mitoses, ulceration, and lymphovascular invasion were independently associated wi

100 mor grade, nodal disease, and perineural and lymphovascular invasion were negative independent predic

101 ge, pN stage, LNR >/=0.2, tumor grade 3, and lymphovascular invasion were significantly associated wi

102 s, ulceration, mitotic rate, regression, and lymphovascular invasion were significantly associated wi

103 ount/mm2 and excluding the optional variable lymphovascular invasion) for each patient.

104 The step of intravasation (lymphovascular invasion), a rate-limiting step in metast

105 f patients undergoing RH for stage IA1 (with lymphovascular invasion), IA2, and IB1 squamous, adenoca

106 al margin positivity, 16 patients (3.9%) for lymphovascular invasion, 13 patients (3.2%) for high-gra

107 e receptor, nuclear grade, histologic grade, lymphovascular invasion, and clinical stage grouping) we

108 h tumor size, depth of invasion, presence of lymphovascular invasion, and degree of tumor differentia

109 C can be used for prediction of tumor grade, lymphovascular invasion, and depth of myometrial invasio

110 r hilum (rete testis and hilar soft tissue), lymphovascular invasion, and elevated preorchiectomy lev

111 uding increased grade, nodal involvement and lymphovascular invasion, and independently predicted bot

112 ameters like tumor size, proliferative rate, lymphovascular invasion, and metastases to lymph nodes.

113 re immunocompetent and had tumors 1.0 cm, no lymphovascular invasion, and negative pathologic margins

114 Tumors that had poor differentiation, lymphovascular invasion, and size >/=2 cm were significa

115 ta were also collected on ulceration status, lymphovascular invasion, and the tumor mitotic rate.

116 h of tumor invasion, tumor size, presence of lymphovascular invasion, and tumor grade.

117 with postoperative disease-free survival and lymphovascular invasion, and was essentially conserved i

118 ed progression and cancer-specific survival (lymphovascular invasion, associated carcinoma in situ, n

119 or age, race, stage, grade, receptor status, lymphovascular invasion, body mass index, diabetes, hype

120 d clear margins; grade 3 tumour histology or lymphovascular invasion, but not both, were permitted),

121 Plasma D-dimer levels were markers of lymphovascular invasion, clinical stage, and lymph node

122 defined by bulky tumors, variant histology, lymphovascular invasion, hydronephrosis and/or high-grad

123 logical level, the depth of tumour invasion, lymphovascular invasion, invasion of large veins, host l

124 ie, tumour size >2 cm, histological grade 3, lymphovascular invasion, Ki67 >20%, age <=35 years, or h

125 lial carcinoma within the prostatic urethra, lymphovascular invasion, micropapillary disease, or hydr

126 isease without receipt of endocrine therapy, lymphovascular invasion, multifocal disease on pathology

127 absence of chronic kidney disease, negative lymphovascular invasion, negative surgical margin, and a

128 ure-extrathyroidal extension, multifocality, lymphovascular invasion, nodal or distant metastasis.

129 or stage pT2N0 with a histologic grade of 3, lymphovascular invasion, or both (tumor size: T1, <=2 cm

130 advanced pathologic stage, low-lying tumor, lymphovascular invasion, or perineural invasion.

131 ng for sex, treatment arm, T-stage, N-stage, lymphovascular invasion, perineural invasion and lymph n

132 statectomy Gleason sum, lymph node invasion, lymphovascular invasion, perineural invasion, and higher

133 signet ring cells, mucinous tumor, budding, lymphovascular invasion, perineural invasion, and lympha

134 umbers of positive and negative lymph nodes, lymphovascular invasion, perineural invasion, and use of

135 ension, tumor thickness, DOI, margin status, lymphovascular invasion, perineural invasion, muscle inv

136 levels and adverse pathology, which included lymphovascular invasion, perineural invasion, or extrano

137 ere not associated with pathologic ENE, PSM, lymphovascular invasion, perineural invasion, or pN2 cat

138 ound between pretreatment fragment level and lymphovascular invasion, perineural invasion, pathologic

139 topathologic subtype, differentiation grade, lymphovascular invasion, perineural invasion, T-stage, N

140 e, histologic type, tumor size, tumor grade, lymphovascular invasion, perineural invasion, type of op

141 odes in the surgical specimen, perineural or lymphovascular invasion, poorly or undifferentiated tumo

142 Lymphovascular invasion, preoperative serum carcinoembry

143 no administration of NAT, high tumor grade, lymphovascular invasion, R1/R2 resection, no adjuvant ch

144 ient age, tumor grade, clinical tumor stage, lymphovascular invasion, resection margin status, and su

145 ned immunodeficient mice without manifesting lymphovascular invasion, this step has been difficult to

146 Age, tumor size, tumor type, lymphovascular invasion, tumor location, multifocality,

147 Lymphovascular invasion, tumor size >/=2 cm, and poor di

148 vement, positive superficial margins, and/or lymphovascular invasion, use of a bolus is recommended,

149 f breast cancer characterized by exaggerated lymphovascular invasion, which is a phenotype recapitula

150 7%/3% of seminoma recurrences, in 48%/38% of lymphovascular invasion-negative and 41%/61% of lymphova

151 ovascular invasion-positive CSI nonseminoma, lymphovascular invasion-negative CSI nonseminoma and CSI

152 nths) and 14 months (range, 2-84 months) for lymphovascular invasion-positive CSI nonseminoma, lympho

153 phovascular invasion-negative and 41%/61% of lymphovascular invasion-positive patients, respectively.

154 le to, or greater than, tumor size, grade or lymphovascular invasion.

155 term disease-free survival in the absence of lymphovascular invasion.

156 T1b, non-high nuclear grade tumors, without lymphovascular invasion.

157 r emboli within lymphovascular spaces called lymphovascular invasion.

158 del with mitotic rate, melanoma subtype, and lymphovascular invasion.

159 ral review of histologic subtype, grade, and lymphovascular invasion.

160 There was extensive lymphovascular invasion.

161 osis between tumor grade and the presence of lymphovascular invasion.

162 breast carcinomas correlates with increased lymphovascular invasion.

163 e, MMR, number of nodes examined, grade, and lymphovascular invasion.

164 inoma, poorly differentiated (grade 3), with lymphovascular invasion.

165 ive correlation between CXCR3 expression and lymphovascular invasion.

166 ller median size, and less frequently showed lymphovascular invasion.

167 are locally invasive and exhibit peritumoral lymphovascular invasion.

168 ocation, or multicentricity; the presence of lymphovascular invasion; histologic or nuclear grade; or

169 prognosis depends on the depth of invasion, lymphovascular involvement, and histological type.

170 e, location,and differentiation, presence of lymphovascular or perineural invasion,mucinous histology

171 logic stage, tumor distance from anal verge, lymphovascular or perineural invasion.

172 ase, resection margins, grade, mesoappendix, lymphovascular, perineural involvement) was found in thi

173 ve lymph nodes and surgical specimens: size, lymphovascular/perineural invasion, and microglandular a

174 ssion analysis showed that stage III cancer, lymphovascular permeation, and blood transfusion, but no

175 pendent of age, sex, pathological stage, and lymphovascular space invasion (coefficient 9.81, 95% CI

176 higher T classification, larger tumor size, lymphovascular space invasion (LVSI), and malignant peri

177 een CA125 levels and the likelihood of +LNM, lymphovascular space invasion (LVSI), grade, and stage.

178 multifocal pattern of residual disease, and lymphovascular space invasion in the specimen.

179 than 2 cm, multifocal residual disease, and lymphovascular space invasion predict higher rates of LR

180 cting tumour biology (histological subtypes, lymphovascular space invasion, and molecular classificat

181 hort including age, tumor grade, FIGO stage, lymphovascular space invasion, and the molecular subgrou

182 ed with tumor histology, primary tumor size, lymphovascular space invasion, extranodal extension, the

183 ecology and Obstetrics (FIGO) stage IA1 with lymphovascular space invasion, IA2, or IB1 adenocarcinom

184 de 3 cancer with deep myometrial invasion or lymphovascular space invasion, or both; stage II or III

185 sociated with higher grade and more frequent lymphovascular space invasion.

186 have higher-grade cancers and more frequent lymphovascular space invasion.

187 nd was associated with a higher frequency of lymphovascular space involvement (76.5 vs. 56.5%, p < 0.

188 ctors (subtype, tumour grade, involvement of lymphovascular space), disease stage (including myometri

189 margin of invasive ductal carcinomas, in the lymphovascular space, and in lymph node metastases.

190 characterized by florid tumor emboli within lymphovascular spaces called lymphovascular invasion.

191 characterized by florid tumor emboli within lymphovascular spaces termed lymphovascular invasion (LV

192 lymphangiomas, congenital hamartomas of the lymphovascular tissue, are often associated with signifi

193 The genesis and unique properties of the lymphovascular tumor embolus are poorly understood large

194 The lymphovascular tumor embolus is a blastocyst-like struct