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1 tumors (0.67% for MCF-7 tumors and 0.77% for endometrial tumors).
2 or immunogenicity and anti-tumor immunity in endometrial tumor.
3 e been found in many sporadic colorectal and endometrial tumors.
4 intracellular signaling pathway activated in endometrial tumors.
5 the etiology of some sporadic colorectal and endometrial tumors.
6 thod of blocking angiogenesis in ovarian and endometrial tumors.
7 ttenuated in a significant fraction of human endometrial tumors.
8  protein-encoding genes in 13 primary serous endometrial tumors.
9 rf2 was compared in different types of human endometrial tumors.
10 tion at the MLH1 promoter within a subset of endometrial tumors.
11 ed with mice bearing MCF-7 and primary human endometrial tumors.
12 served in patients with breast, ovarian, and endometrial tumors.
13 rongly expressed on esophageal, gastric, and endometrial tumors.
14 is associated with an increased incidence of endometrial tumors.
15 s as malignancy increases in both breast and endometrial tumors.
16 rowth pattern, lymphoma, mammary tumors, and endometrial tumors.
17 d absent or reduced in a majority of primary endometrial tumors.
18 n ligase is mutated in at least 16% of human endometrial tumors.
19 CC) as well as in 20% of presumably sporadic endometrial tumors.
20 one in inhibiting progression of early-stage endometrial tumors.
21 ssion of ARID1A protein in endometrioid-type endometrial tumors.
22 as (113 patients with colorectal tumors, 178 endometrial tumors); 100% of double somatic cases had a
23  to the development of poorly differentiated endometrial tumors, a lethal form of cancer.
24 ll lines (n = 6) and 68% of 117 endometrioid endometrial tumors analyzed.
25                              Comparing human endometrial tumors and cells with their nonmalignant cou
26  showed that survivin was hypermethylated in endometrial tumors and correlated with increased survivi
27 led a new mode of PI3K alteration in primary endometrial tumors and warrants future studies to determ
28 eased EMX2 expression in a subset of primary endometrial tumors, and four of six endometrial cancer c
29 epithelial ovarian cancers (EOCs), cervical, endometrial tumors, and uterine sarcomas that are genomi
30 ed expression of PRL receptor in ovarian and endometrial tumors as well as in endometrial hyperplasia
31 endometase gene was only obtained from human endometrial tumor cDNA library.
32 umors, a colon tumor cell line (SW48) and an endometrial tumor cell line (AN3CA), did not express hML
33                                          The endometrial tumor cell line HEC59 contains mutations in
34 breast, prostate, colon, lung, cervical, and endometrial tumor cells in culture to undergo apoptosis
35 ial response to progestins in differentiated endometrial tumor cells results in part from binding of
36 motes migration and invasion of PTEN-deleted endometrial tumor cells.
37            Levels of Cyr61 were decreased in endometrial tumors compared with normal endometrium.
38                         Gastrointestinal and endometrial tumors comprise a separate cluster for which
39  26 (MMP-26) (matrixin) gene, endometase, an endometrial tumor-derived metalloproteinase.
40                                          The endometrial tumors develop only in Alk5 cKO mice that ar
41 e controlled by Arid1a and have an impact on endometrial tumor development.
42 Ralpha-binding sites in tamoxifen-associated endometrial tumors differed from those in the tumors fro
43  a subset of unselected gastrointestinal and endometrial tumors exhibit a microsatellite mutator phen
44                                  Colonic and endometrial tumors from HNPCC patients exhibit microsate
45         While the MSI+ phenotype observed in endometrial tumors from HNPCC patients is attributed to
46 umors from tamoxifen users with those of six endometrial tumors from nonusers and integrated these re
47 dometrial tumors from tamoxifen users and 64 endometrial tumors from nonusers.
48 e results with the transcriptomic data of 47 endometrial tumors from tamoxifen users and 64 endometri
49 seq), we compared the ERalpha profiles of 10 endometrial tumors from tamoxifen users with those of si
50 ERalpha transcriptional action in breast and endometrial tumors have been found that might explain th
51 s been repeatedly observed in colorectal and endometrial tumors in previous studies despite many poss
52                                              Endometrial tumors in raloxifene users had a more favora
53 ere observed in one breast carcinoma and one endometrial tumor; in at least one of these cases, tumor
54 s-of-function CTCF mutation in >20% of human endometrial tumors indicates its importance in uterine h
55        PRL mRNA was expressed in ovarian and endometrial tumors, indicating the presence of an autocr
56 206H mutation is also present in a subset of endometrial tumors, melanomas, non-small lung cancers, a
57 multiple ARID1A mutant bladder, ovarian, and endometrial tumor models and improved cisplatin response
58 was found to be overexpressed (P < 0.005) in endometrial tumors (n = 74) compared with uninvolved con
59  the general population and characterize the endometrial tumors occurring in these groups.
60 ggering long-term silencing of these loci in endometrial tumors of obese patients.
61  FGFR2 may be a viable therapeutic option in endometrial tumors possessing activating mutations in FG
62 ingle-cell resolution from human ovarian and endometrial tumors processed immediately following surgi
63 hts into how ARID1A inactivation accelerates endometrial tumor progression and dissemination, the maj
64 esults demonstrated that Pten/Lkb1-deficient endometrial tumors rely strongly on deregulated mTOR sig
65 r) nu/nu mice bearing GPR30-expressing human endometrial tumors revealed GPR30-mediated uptake of the
66       Finally, examination of DICER1 hotspot endometrial tumors reveals derepression of specific miRN
67 expression but not with HNF1B methylation in endometrial tumor samples from The Cancer Genome Atlas.
68   There is a wide range of aggressiveness of endometrial tumors, some being indolent and easily treat
69  Immunohistochemical analysis of 230 primary endometrial tumor specimens showed that lack of FOXA1 an
70 , our findings demonstrated that FOXA2 is an endometrial tumor suppressor associated with aggressive
71 allelic deletion corresponding to a putative endometrial tumor suppressor at 10q26.
72 on of miR-129-2 was lost in 27 of 31 primary endometrial tumors that also showed a concomitant gain o
73  Our study highlights the divergence between endometrial tumors that arise in different hormonal cond
74 binding signature of ERalpha differs between endometrial tumors that arise in the presence or absence
75        The LUS group consisted of women with endometrial tumors that clearly originated between the l
76                   However, the metabolism of endometrial tumors themselves has been largely understud
77 ic target for sensitizing hormone-refractory endometrial tumors to progesterone therapy.
78              As survivin is overexpressed in endometrial tumors, we hypothesized that hypomethylation
79 , we identified patients with colorectal and endometrial tumors who had 2 or more somatic (but not ge
80 ive with a Lynch syndrome-associated cancer, endometrial tumor with loss of MSH2 expression, tumors w
81                         A hormone-refractory endometrial tumor with low levels of stromal PR develope
82 o rapid development of advanced endometrioid endometrial tumors with 100% penetrance and short host s
83             Most patients with colorectal or endometrial tumors with 2 or more somatic (but not germl
84                  Hypermutable colorectal and endometrial tumors with functional MMR were recently rep
85                                Indeed, using endometrial tumors with immunohistochemically proven MMR
86                          Some colorectal and endometrial tumors with microsatellite instability not a