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1 nism for hormone-independent pathogenesis of endometrial adenocarcinoma.
2 NA genesis, also plays a significant role in endometrial adenocarcinoma.
3             Five had thymomas and one had an endometrial adenocarcinoma.
4 with E2 developed invasive endometrioid-type endometrial adenocarcinoma.
5 ineered mouse model of poorly differentiated endometrial adenocarcinoma.
6 y medications (NSAID), and acetaminophen and endometrial adenocarcinoma.
7 ease states such as renal cell carcinoma and endometrial adenocarcinoma.
8 ls, derived from a well-differentiated human endometrial adenocarcinoma.
9 allele spontaneously develop highly invasive endometrial adenocarcinomas.
10 hich are premalignant precursors of invasive endometrial adenocarcinomas.
11                             One patient with endometrial adenocarcinoma achieved a complete response
12                One patient with endometrioid endometrial adenocarcinoma achieved a CR and remained on
13 hysterectomies with both well-differentiated endometrial adenocarcinoma and adjacent (normal or abnor
14 However, these mice did not develop invasive endometrial adenocarcinoma, and instead succumbed premat
15 -menopausal endometrium, well-differentiated endometrial adenocarcinoma, and poorly differentiated ma
16                                              Endometrial adenocarcinoma arises from the uncontrolled
17 gresses to endometrial carcinoma in situ and endometrial adenocarcinoma as evidenced by myometrial in
18         These lesions progressed to invasive endometrial adenocarcinomas as early as 9 months of age
19 by RNA interference in a well differentiated endometrial adenocarcinoma cell line (Ishikawa) stimulat
20 ne responsiveness, and differentiation of an endometrial adenocarcinoma cell line (Ishikawa).
21  cell line HCT-116 and sublines of the human endometrial adenocarcinoma cell line HEC59.
22 ter expression in the Ishikawa human uterine endometrial adenocarcinoma cell line.
23 tor-dependent p38 activation by estrogens in endometrial adenocarcinoma cells and in vitro and in viv
24 ell proliferation and invasive phenotypes in endometrial adenocarcinoma cells, where it helps maintai
25 ked highly invasive and sometimes metastatic endometrial adenocarcinomas closely resembling those obs
26 Committee on Cancer stage IA-C node-negative endometrial adenocarcinoma comprised the study populatio
27  tumors are hypothesized to develop from the endometrial adenocarcinoma (EAC) through epithelial-mese
28    Normal proliferative, EIN, and malignant (endometrial adenocarcinoma) endometrial tissues were imm
29                                              Endometrial adenocarcinomas exhibited changes in the lev
30 ters early uterine morphogenesis and induces endometrial adenocarcinomas in adults.
31                                              Endometrial adenocarcinoma is the most common gynecologi
32 currently shown, treatment of cultured human endometrial adenocarcinoma (Ishikawa) cells with resvera
33 he most common histologies were endometrioid endometrial adenocarcinoma (n = 13), prostate adenocarci
34 alysis to date of adjuvant RT in early stage endometrial adenocarcinoma, our study reveals a statisti
35                     In clinical specimens of endometrial adenocarcinoma, PME-1 levels were increased
36 f adjuvant radiation therapy (RT) in stage I endometrial adenocarcinoma remains controversial despite
37                     We used a mouse model of endometrial adenocarcinoma that results from brief devel
38 l endometrial proliferation and, ultimately, endometrial adenocarcinoma, the fourth most common cance
39 ncer cell lines from multiple origins and in endometrial adenocarcinoma tumors, there appears to be n
40 en in mice resulted in poorly differentiated endometrial adenocarcinomas, which expressed Napsin A an
41 rone receptor cre ("Alk5 cKO") that develops endometrial adenocarcinoma with metastasis to the lungs.
42      These tumors were poorly differentiated endometrial adenocarcinomas with prominent nuclear atypi