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1 ing-mimicking diet prevent tamoxifen-induced endometrial hyperplasia.
2  growth and function, and the development of endometrial hyperplasia.
3 nths of age, the absence of Mig-6 results in endometrial hyperplasia.
4 ma, prostatic intraepithelial neoplasia, and endometrial hyperplasia.
5 ortant, since unexpected bleeding may signal endometrial hyperplasia.
6  the mechanism by which tamoxifen results in endometrial hyperplasia.
7  accompanied by an unacceptably high rate of endometrial hyperplasia.
8 ocrine therapy and reduces tamoxifen-induced endometrial hyperplasia, a strategy with potential clini
9 and was restricted primarily to the atypical endometrial hyperplasia (AEH) type with coexisting endom
10  measure was endometrial cancer and atypical endometrial hyperplasia (AEH).
11  cytological features are abnormal, atypical endometrial hyperplasia (AEH).
12 of TGFbetaR2 resulted in female infertility, endometrial hyperplasia, altered estrogen and progestero
13  lost in a high percentage of cases of human endometrial hyperplasia and adenocarcinoma, which are li
14 and phosphorylated ER-alpha was increased in endometrial hyperplasia and atypical hyperplasia compare
15  to female reproductive disorders, including endometrial hyperplasia and breast cancer.
16 cated as a mediator of the increased risk of endometrial hyperplasia and cancer resulting from the us
17 dometrium cooperates with Pten loss to drive endometrial hyperplasia and cancer.
18   Cables mutant mice are viable, but develop endometrial hyperplasia and carcinoma in situ at a young
19  important implications for the treatment of endometrial hyperplasia and carcinoma in women.
20 nting the pathogenesis of conditions such as endometrial hyperplasia and endometrial cancer.
21 osity in stromal APC is sufficient to induce endometrial hyperplasia and endometrial carcinogenesis b
22 e cellular proliferation in vivo in atypical endometrial hyperplasia and endometrial endometrioid ade
23         Wnt7a(cre+)Mig-6(f/f) mice developed endometrial hyperplasia and estrogen-dependent endometri
24 he murine uterus leads to the development of endometrial hyperplasia and estrogen-induced endometrial
25                    Our findings show that in endometrial hyperplasia and low-grade EEC, coordinate in
26 te the clinical value of ALDH1 expression in endometrial hyperplasia and to determine its ability to
27 had opposite effects for endometrial cancer, endometrial hyperplasia, and Alzheimer disease.
28 oxifen include vaginal endometrial bleeding, endometrial hyperplasia, and cancer, conditions associat
29 esions allowed us to exclude polyps, but not endometrial hyperplasias, as potential precancers.
30 ession on a TMA, including a large series of endometrial hyperplasia, atypical hyperplasia, and adeno
31 pression showed a step-wise increase between endometrial hyperplasia, atypical hyperplasia, and endom
32 8.9% of Pten(+/-)ERalpha(-/-) mice developed endometrial hyperplasia/carcinoma.
33                   Female mutant mice develop endometrial hyperplasia due to aberrant phosphorylation
34 nt in endometrial tumorigenesis we evaluated endometrial hyperplasia (EH) characterized as simple, co
35                                              Endometrial hyperplasia (EH) is a precusor lesion for en
36 en and progesterone bear on the incidence of endometrial hyperplasia (EH), a noninvasive proliferatio
37                      PURPOSE The severity of endometrial hyperplasia (EH)-simple (SH), complex (CH),
38 etrial carcinoma and its precursor, atypical endometrial hyperplasia (EH).
39 able evidence that tamoxifen can also induce endometrial hyperplasia in pre menopausal women.
40 ar tissue, classified as either non-atypical endometrial hyperplasia (NEH) or, if the cytological fea
41               These females develop atypical endometrial hyperplasia of which approximately 20% progr
42 omplex structures, such as those observed in endometrial hyperplasia or carcinoma.
43 ogy clinics in Manchester, UK, with atypical endometrial hyperplasia or endometrial endometrioid aden
44  may present with vaginal bleeding caused by endometrial hyperplasia or uterine cancer as a result of
45 R+ putative endometrial precancers (atypical endometrial hyperplasias) progress to RER+ carcinomas, w
46 ovarian and endometrial tumors as well as in endometrial hyperplasia, signifying the importance of PR
47            Endometrial cancer is preceded by endometrial hyperplasia, unopposed estrogen exposure, an
48                          Genomic DNA from 51 endometrial hyperplasias was extracted from paraffin blo
49 plasms of uncertain malignant potential, and endometrial hyperplasia were estimated.
50  tumors of uncertain malignant potential, or endometrial hyperplasia) were 0.67% (n = 257) (95% CI, 0
51  carcinoma, endometrial polyps, and atypical endometrial hyperplasias, whereas normal and anovulatory
52 d estrogen stimulation is thought to lead to endometrial hyperplasia which precedes malignant progres
53 e whether PTEN mutations also are present in endometrial hyperplasias, which are premalignant precurs
54 endent prognostic indicator of patients with endometrial hyperplasia with or without atypia who would
55 ved human specimens of normal endometrium; 7 endometrial hyperplasia with or without atypia; 32 endom
56 was no higher frequency of PTEN mutations in endometrial hyperplasias with atypia (6 of 32; 19%) rela
57                                              Endometrial hyperplasia worsened with age, and all Smad2