ライフサイエンスコーパス: invasive breast carcinoma

1 ed to tamoxifen or no-adjuvant treatment for invasive breast carcinoma.

2 (DCIS) is a noninvasive precursor lesion to invasive breast carcinoma.

3 r most women with hormone receptor positive, invasive breast carcinoma.

4 Nm23-H1, known to be downregulated in human invasive breast carcinoma.

5 All women had primary, invasive breast carcinoma.

6 nd HER2/neu were found to be co-expressed in invasive breast carcinomas.

7 elevated in approximately 80% of in situ and invasive breast carcinomas.

8 ression of phospho-BRCA1 (Ser1423) in 39% of invasive breast carcinomas.

9 levels of BRCA1 tumor suppressor protein in invasive breast carcinomas.

10 ession of phospho-Akt-1 (Ser(473)) in 21% of invasive breast carcinomas.

11 yrosine kinase overexpressed in about 25% of invasive breast carcinomas.

12 rmal breast epithelia but is up-regulated in invasive breast carcinomas.

13 s from normal breast tissue, and in situ and invasive breast carcinomas.

14 or as much as 50% of the total tumor mass in invasive breast carcinomas.

15 andidate "second hits" in the development of invasive breast carcinomas.

16 uctal carcinomas of the breast as well as in invasive breast carcinomas.

17 epithelial and stromal DNA from 134 sporadic invasive breast carcinomas.

18 romal and epithelial compartments of primary invasive breast carcinomas.

19 revealed expression of Cyr61 in about 30% of invasive breast carcinomas.

20 east cancer cells is highly overexpressed in invasive breast carcinomas.

21 itu hybridization technique, we analyzed 114 invasive breast carcinomas, 29 carcinoma in situ lesions

22 ip1 occur in cancer, we screened 53 cases of invasive breast carcinoma, 35 cases of ductal carcinoma

23 uamous cell carcinomas and adjacent tissues, invasive breast carcinomas, adjacent tissues and normal

24 Histopathologic findings of primary invasive breast carcinoma and local recurrence are usual

25 related protein 1 (Drp1) expression in human invasive breast carcinoma and metastases to lymph nodes.

26 st this theory, 68 patients with 69 operable invasive breast carcinomas and clinically node-negative

27 permethylated in six out of 32 (19%) primary invasive breast carcinomas and eight out of 44 (18%) pri

28 eduction of CCN6 expression occurs in 60% of invasive breast carcinomas and is associated with axilla

29 r cancer represents approximately 10% of all invasive breast carcinomas and is often poorly defined o

30 RNA is overexpressed in approximately 50% of invasive breast carcinomas and promotes tumor progressio

31 s reduced or lost in a substantial number of invasive breast carcinomas and that CCN6 modulates trans

32 e that specific TN isoforms are expressed in invasive breast carcinomas and that these isoforms are i

33 epithelium resulted in development of highly invasive breast carcinomas and the formation of whole ch

34 for genetic alterations in PIK3CA have been invasive breast carcinomas and the frequency of PIK3CA m

35 entified a SAGE tag that was present only in invasive breast carcinomas and their lymph node metastas

36 1 normal breast tissues, 17 noninvasive, 151 invasive breast carcinomas, and 6 cell lines by in-house

37 expression in benign breast tissues, primary invasive breast carcinomas, and metastatic breast carcin

38 OX-2 in promoting the progression of DCIS to invasive breast carcinomas, and suggest that therapeutic

39 uding 10 ductal carcinoma in situ (DCIS), 18 invasive breast carcinomas, and two lymph node metastase

40 essions of which are aberrantly increased in invasive breast carcinomas as compared with adjacent nor

41 o GTPase family that have been implicated in invasive breast carcinomas, attributing specific functio

42 nt transactivation of EGFR and ErbB2/HER2 in invasive breast carcinoma, but not in normal mammary epi

43 ession of ductal carcinoma in situ (DCIS) to invasive breast carcinomas by using a xenograft model of

44 RhoC is specifically expressed in invasive breast carcinomas capable of metastasizing, and

45 Using our device, we performed tests on 76 invasive breast carcinoma cases expressing various level

46 umorigenic breast cell line, MCF10A, and the invasive breast carcinoma cell line, MDA-MB-231.

47 ve demonstrated the loss of EphB6 protein in invasive breast carcinoma cell lines and absence of EphB

48 oviral RNA interference approach to generate invasive breast carcinoma cells (SUM-159 cells) that lac

49 selectively up-regulated and coexpressed in invasive breast carcinoma cells, where, upon physical in

50 ASH) on MT1-MMP-containing late endosomes in invasive breast carcinoma cells.

51 of 17 markers by immunohistochemistry in 842 invasive breast carcinomas collected in a population-bas

52 pt and protein were consistently elevated in invasive breast carcinoma compared with normal breast ep

53 6B expression was significantly increased in invasive breast carcinoma compared with normal breast ti

54 ur findings indicate that fibroblasts within invasive breast carcinomas contribute to tumor promotion

55 eatly decreased in 70% of 30 human sporadic, invasive breast carcinomas examined by immunocytochemist

56 d with BMP4 and phospho-p38 levels in 69% of invasive breast carcinomas examined, consistent with the

57 Although p53 mutations are common in invasive breast carcinoma, few have been identified in b

58 We studied 48 cases of invasive breast carcinoma for evidence of Epstein-Barr v

59 pithelium and stroma of 220 primary sporadic invasive breast carcinomas for global genomic alteration

60 oud sequencing data are available, and on an invasive breast carcinoma genome that we sequenced using

61 e clinical importance of CSF-1 and CSF-1R in invasive breast carcinoma has been recognized, but the s

62 cinoma in situ (DCIS) and its progression to invasive breast carcinoma have not been defined.

63 Two subgroups of invasive breast carcinomas have been identified with a p

64 d in ductal carcinoma in situ (DCIS) than in invasive breast carcinomas (IBC), suggesting a potential

65 ow that LMO7 is upregulated in the stroma of invasive breast carcinoma in a manner that correlates wi

66 al enrolled women with clinical T1 to T2N0M0 invasive breast carcinoma in a prospective observational

67 mmon in normal breast epithelium adjacent to invasive breast carcinoma in BRCA1-linked cases compared

68 ence of EBV infection in tissues involved by invasive breast carcinomas in a significant subset of ca

69 basal-like subgroup in a set of 297 primary invasive breast carcinomas in which the staining profile

70 sis identified 103 SAGE tags as specific for invasive breast carcinomas, in comparison with in situ d

71 DCD is overexpressed in approximately 10% of invasive breast carcinomas; in some cases its overexpres

72 ally, we demonstrate that PAR1 expression in invasive breast carcinoma is essential for tumor growth

73 einvasive ductal carcinoma in situ (DCIS) to invasive breast carcinoma is marked by infiltration of s

74 US-guided percutaneous ablation of small invasive breast carcinomas is feasible and safe.

75 ria: 200 or more node-negative patients with invasive breast carcinoma; median follow-up time at leas

76 ingly, HRG expression in tumor biopsies from invasive breast carcinomas (n = 189) revealed that, wher

77 tained, 102 were subsequently diagnosed with invasive breast carcinoma, nine were subsequently diagno

78 st AS at a median 85 months from surgery for invasive breast carcinoma or ductal carcinoma in situ.

79 examined JAB1 and p27 protein expression in invasive breast carcinoma specimens and the association

80 unohistochemical staining of a cohort of 100 invasive breast carcinoma specimens.

81 ers were significantly higher in in situ and invasive breast carcinomas than in normal breast; invasi

82 In invasive breast carcinoma, there is a positive relations

83 protein, however, are low or undetectable in invasive breast carcinoma tissue and cell lines.

84 Overexpression of EZH2 has been detected in invasive breast carcinoma tissue samples and is observed

85 resections or tissue microarrays (TMAs) from invasive breast carcinoma tissue were tested by both IHC

86 ntial therapeutic target for preinvasive and invasive breast carcinoma treatment.

87 tive series of 202 patients with stage T1a,b invasive breast carcinomas was evaluated.

88 amoxifen trial cohort including in total 564 invasive breast carcinomas, we examined TGFBR2 expressio

89 One hundred cases of invasive breast carcinoma were evaluated for which FISH

90 Eleven women with invasive breast carcinoma were imaged with DOS tomograph

91 Seventy-four consecutive women with invasive breast carcinoma were recruited to undergo preo

92 d be useful to identify patients with small, invasive breast carcinomas who might benefit from adjuva