ライフサイエンスコーパス: lymphovascular invasion

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

2 There was extensive lymphovascular invasion.

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

4 breast carcinomas correlates with increased lymphovascular invasion.

5 ive correlation between CXCR3 expression and lymphovascular invasion.

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

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

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

9 are locally invasive and exhibit peritumoral lymphovascular invasion.

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

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

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

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

14 r emboli within lymphovascular spaces called lymphovascular invasion.

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

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

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

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

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

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

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

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

23 39, 4: OR 4.15, X: OR 1.87), and presence of lymphovascular invasion (absent: reference, present: OR

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

64 Lymphovascular invasion in the orchiectomy specimen, a h

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

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

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

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

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

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

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

72 Lymphovascular invasion (LVI) was the only clinicopathol

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

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

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

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

77 26 (IQR, 19-34); perineural invasion (PNI), lymphovascular invasion (LVI), and residual positive mar

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

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

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

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

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

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

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

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

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

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

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

89 7%/3% of seminoma recurrences, in 48%/38% of lymphovascular invasion-negative and 41%/61% of lymphova

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

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

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

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

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

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

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

97 [95% CI, 1.22-1.48]; P < .001), presence of lymphovascular invasion (OR, 1.26 [1.19-1.33]; P < .001)

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

130 Lymphovascular invasion, preoperative serum carcinoembry

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

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

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

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

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

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

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

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

139 Lymphovascular invasion was present.

140 Lymphovascular invasion was the only significant factor

141 Pathologic stage and lymphovascular invasion were independent predictors of D

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

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

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

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

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