ライフサイエンスコーパス: lymphovascular invasion

1 There was extensive lymphovascular invasion.

2 breast carcinomas correlates with increased lymphovascular invasion.

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

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

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

6 are locally invasive and exhibit peritumoral lymphovascular invasion.

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

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

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

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

11 r emboli within lymphovascular spaces called lymphovascular invasion.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

40 Lymphovascular invasion (LVI) was the only clinicopathol

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

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

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

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

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

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

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

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

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

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

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

52 7%/3% of seminoma recurrences, in 48%/38% of lymphovascular invasion-negative and 41%/61% of lymphova

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

75 Lymphovascular invasion, preoperative serum carcinoembry

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

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

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

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

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

81 Lymphovascular invasion was the only significant factor

82 Pathologic stage and lymphovascular invasion were independent predictors of D

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

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

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