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1 mesothelioma, pancreatic adenocarcinoma, and ovarian adenocarcinoma.
2 ain, melanoma, invasive ductal carcinoma and ovarian adenocarcinoma.
3 bservation made in a wide selection of human ovarian adenocarcinomas.
4 ogical markers for distinguishing colon from ovarian adenocarcinomas.
5 deletions is also observed in prostatic and ovarian adenocarcinomas.
6 potential (LMP) and 66 classified as primary ovarian adenocarcinomas].
7 d frequent loss of p27 expression in primary ovarian adenocarcinomas (33%), with respect to LMP tumor
9 nes aberrantly expressed in serous papillary ovarian adenocarcinoma and may be useful for the identif
10 (O/E, 1.29; 95% CI, 1.06-1.56) and mucinous ovarian adenocarcinoma and rectal cancer (OE/E, 1.95; 95
11 s, has a broad expression range in colon and ovarian adenocarcinomas, and may behave as a biomarker f
12 adenocarcinoma; SKVLB a multidrug resistant ovarian adenocarcinoma; and HT-29, a colon carcinoma).
14 (25 of 32) of breast and 44% (76 of 171) of ovarian adenocarcinoma as assessed by in situ hybridizat
16 d (ATRA) treatment of the retinoid-sensitive ovarian adenocarcinoma cell line CAOV3, but not the reti
18 coprotein (P-gp) gene silencing in the human ovarian adenocarcinoma cell line, NCI-ADR/Res (NAR), ove
21 physiological setting, TGF-beta insensitive ovarian adenocarcinoma cells (HEY) have a very low GULP
23 in two living human tumor cell lines: Caov-3 ovarian adenocarcinoma cells and A-498 kidney carcinoma
24 ention of 8 and 13 in ip xenografts of human ovarian adenocarcinoma cells NIH:OVCAR-3, which overexpr
25 nomic dsDNA breaks (DSBs) were identified in ovarian adenocarcinoma cells using immunodetection of ga
26 endometrial carcinoma cells), OVCAR-3 (human ovarian adenocarcinoma cells), EM42 (human endometrial e
27 a cells, COS-1 cells, HeLa cells, or SK-OV-3 ovarian adenocarcinoma cells, all of which do not expres
30 that rhuCD40L inhibits the growth of several ovarian adenocarcinomas derived from surgical specimens
31 pies, including hepatocellular carcinoma and ovarian adenocarcinoma, Gadd45b inhibition in myeloid ce
33 of peritoneal endometriosis and endometrioid ovarian adenocarcinoma in mice, both based on the activa
34 cy in the United States, and advanced serous ovarian adenocarcinoma is responsible for most ovarian c
35 ogical association between endometriosis and ovarian adenocarcinoma may be attributable to shared gen
37 ta indicate that gene expression patterns in ovarian adenocarcinomas reflect both morphological featu
38 ethods: Human pleural mesothelioma (I45) and ovarian adenocarcinoma (SKOV3) cell lines were engineere
39 different human tumor cell lines (SKOV3, an ovarian adenocarcinoma; SKVLB a multidrug resistant ovar
40 invasive and widely metastatic endometrioid ovarian adenocarcinomas with complete penetrance and a d
41 de, which caused tumor regression in a human ovarian adenocarcinoma xenograft model with on-pathway b
42 les were quantified in 42 mice bearing human ovarian adenocarcinoma xenograft tumors by use of a high