ライフサイエンスコーパス: endometrial tumor

1 tumors (0.67% for MCF-7 tumors and 0.77% for endometrial tumors).

2 intracellular signaling pathway activated in endometrial tumors.

3 the etiology of some sporadic colorectal and endometrial tumors.

4 thod of blocking angiogenesis in ovarian and endometrial tumors.

5 ttenuated in a significant fraction of human endometrial tumors.

6 e been found in many sporadic colorectal and endometrial tumors.

7 protein-encoding genes in 13 primary serous endometrial tumors.

8 rf2 was compared in different types of human endometrial tumors.

9 tion at the MLH1 promoter within a subset of endometrial tumors.

10 ed with mice bearing MCF-7 and primary human endometrial tumors.

11 served in patients with breast, ovarian, and endometrial tumors.

12 rongly expressed on esophageal, gastric, and endometrial tumors.

13 is associated with an increased incidence of endometrial tumors.

14 s as malignancy increases in both breast and endometrial tumors.

15 rowth pattern, lymphoma, mammary tumors, and endometrial tumors.

16 d absent or reduced in a majority of primary endometrial tumors.

17 n ligase is mutated in at least 16% of human endometrial tumors.

18 CC) as well as in 20% of presumably sporadic endometrial tumors.

19 as (113 patients with colorectal tumors, 178 endometrial tumors); 100% of double somatic cases had a

20 to the development of poorly differentiated endometrial tumors, a lethal form of cancer.

21 ll lines (n = 6) and 68% of 117 endometrioid endometrial tumors analyzed.

22 Comparing human endometrial tumors and cells with their nonmalignant cou

23 showed that survivin was hypermethylated in endometrial tumors and correlated with increased survivi

24 led a new mode of PI3K alteration in primary endometrial tumors and warrants future studies to determ

25 eased EMX2 expression in a subset of primary endometrial tumors, and four of six endometrial cancer c

26 ed expression of PRL receptor in ovarian and endometrial tumors as well as in endometrial hyperplasia

27 endometase gene was only obtained from human endometrial tumor cDNA library.

28 umors, a colon tumor cell line (SW48) and an endometrial tumor cell line (AN3CA), did not express hML

29 The endometrial tumor cell line HEC59 contains mutations in

30 breast, prostate, colon, lung, cervical, and endometrial tumor cells in culture to undergo apoptosis

31 Levels of Cyr61 were decreased in endometrial tumors compared with normal endometrium.

32 26 (MMP-26) (matrixin) gene, endometase, an endometrial tumor-derived metalloproteinase.

33 Ralpha-binding sites in tamoxifen-associated endometrial tumors differed from those in the tumors fro

34 a subset of unselected gastrointestinal and endometrial tumors exhibit a microsatellite mutator phen

35 Colonic and endometrial tumors from HNPCC patients exhibit microsate

36 While the MSI+ phenotype observed in endometrial tumors from HNPCC patients is attributed to

37 umors from tamoxifen users with those of six endometrial tumors from nonusers and integrated these re

38 dometrial tumors from tamoxifen users and 64 endometrial tumors from nonusers.

39 e results with the transcriptomic data of 47 endometrial tumors from tamoxifen users and 64 endometri

40 seq), we compared the ERalpha profiles of 10 endometrial tumors from tamoxifen users with those of si

41 ERalpha transcriptional action in breast and endometrial tumors have been found that might explain th

42 s been repeatedly observed in colorectal and endometrial tumors in previous studies despite many poss

43 Endometrial tumors in raloxifene users had a more favora

44 ere observed in one breast carcinoma and one endometrial tumor; in at least one of these cases, tumor

45 PRL mRNA was expressed in ovarian and endometrial tumors, indicating the presence of an autocr

46 was found to be overexpressed (P < 0.005) in endometrial tumors (n = 74) compared with uninvolved con

47 the general population and characterize the endometrial tumors occurring in these groups.

48 FGFR2 may be a viable therapeutic option in endometrial tumors possessing activating mutations in FG

49 esults demonstrated that Pten/Lkb1-deficient endometrial tumors rely strongly on deregulated mTOR sig

50 r) nu/nu mice bearing GPR30-expressing human endometrial tumors revealed GPR30-mediated uptake of the

51 expression but not with HNF1B methylation in endometrial tumor samples from The Cancer Genome Atlas.

52 There is a wide range of aggressiveness of endometrial tumors, some being indolent and easily treat

53 Immunohistochemical analysis of 230 primary endometrial tumor specimens showed that lack of FOXA1 an

54 allelic deletion corresponding to a putative endometrial tumor suppressor at 10q26.

55 on of miR-129-2 was lost in 27 of 31 primary endometrial tumors that also showed a concomitant gain o

56 Our study highlights the divergence between endometrial tumors that arise in different hormonal cond

57 binding signature of ERalpha differs between endometrial tumors that arise in the presence or absence

58 The LUS group consisted of women with endometrial tumors that clearly originated between the l

59 However, the metabolism of endometrial tumors themselves has been largely understud

60 ic target for sensitizing hormone-refractory endometrial tumors to progesterone therapy.

61 As survivin is overexpressed in endometrial tumors, we hypothesized that hypomethylation

62 , we identified patients with colorectal and endometrial tumors who had 2 or more somatic (but not ge

63 ive with a Lynch syndrome-associated cancer, endometrial tumor with loss of MSH2 expression, tumors w

64 A hormone-refractory endometrial tumor with low levels of stromal PR develope

65 o rapid development of advanced endometrioid endometrial tumors with 100% penetrance and short host s

66 Most patients with colorectal or endometrial tumors with 2 or more somatic (but not germl

67 Hypermutable colorectal and endometrial tumors with functional MMR were recently rep

68 Indeed, using endometrial tumors with immunohistochemically proven MMR

69 Some colorectal and endometrial tumors with microsatellite instability not a