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1  protects from high fat diet (HFD)-dependent hepatic cancer.
2 lost or significantly downregulated in human hepatic cancer.
3  inactivation of nrf1 in the liver developed hepatic cancer.
4 A system to treat patients with unresectable hepatic cancer.
5 c fungal substances and strongly involved on hepatic cancer.
6 d CaMKIV may represent potential targets for hepatic cancer.
7 alternative in the treatment of unresectable hepatic cancers.
8 eful therapeutic targets in the treatment of hepatic cancers.
9 ng treatment-refractory KRAS-mutant CRC, and hepatic cancers.
10 tions in LS incidence within endometrial and hepatic cancers.
11 ted deaths, 373 (22.9%) due to non-AIDS, non-hepatic cancers, 166 (10.2%) liver-related deaths, and 1
12              CCA accounts for 10% of primary hepatic cancers and is characterized by its aggressive n
13  tumor types including breast, prostate, and hepatic cancers, as well as the process of bone metastas
14 gulates FASN in mice livers and in the HepG2 hepatic cancer cell line.
15 ly hFX increased transduction of several non-hepatic cancer cell lines and Chinese hamster ovary (CHO
16 KK2 protein is highly expressed in all eight hepatic cancer cell lines evaluated and is markedly up-r
17 ver cancers and mitochondria from tumors and hepatic cancer cell lines exhibit VDAC2- and Bak-depende
18 el of liver cancer progression as well as in hepatic cancer cell lines.
19 C), in part, may be owing to the presence of hepatic cancer cells with stem/progenitor features.
20 4 and downregulated IDO1 in tumor-initiating hepatic cancer cells.
21 n results in significant regression of bulky hepatic cancers confined to the liver in the majority of
22 r Liver transplantation (LTx), recurrence of hepatic cancer, de novo cancers, and donor-transmitted c
23 et-induced metabolic syndromes can influence hepatic cancer development.
24 decreased, whereas deaths from non-AIDS, non-hepatic cancers increased and cardiovascular-related dea
25 vel bacterium may cause an increased risk of hepatic cancer induction in susceptible strains of mice.
26                                              Hepatic cancer is one of the most lethal cancers worldwi
27                                The change in hepatic cancer-related gene expression profiles due to R
28                       Genes analyzed include hepatic cancer stem cell markers BAMBI, DKK1,2, DLK1, Ep
29 orting-isolated EpCAM(+) HCC cells displayed hepatic cancer stem cell-like traits including the abili
30 ences of c-MYC activation for the biology of hepatic cancer stem cells (CSC) are undefined.
31 ochondria by autophagy, positively regulates hepatic cancer stem cells (CSCs) by suppressing the tumo
32                                              Hepatic cancer stem cells (HCSCs) are considered as main
33 , only the former is expressed dominantly in hepatic cancer stem cells and correlates significantly t
34 upregulation occurs in HBV-mediated HCCs and hepatic cancer stem cells, by a mechanism not understood
35 t hubs as candidate regulators for targeting hepatic cancer stemness such as, miR-148a, miR-214, E2F
36 tocellular carcinoma (FLC) is a rare primary hepatic cancer that develops in children and young adult
37 ethylation sensitizes subsets of gastric and hepatic cancers to asparaginase therapy.
38 e resections for esophageal, pancreatic, and hepatic cancer were performed at high volume centers, bu
39 tality rates for esophageal, pancreatic, and hepatic cancers were inversely related to hospital volum
40 of patients with esophageal, pancreatic, and hepatic cancers were treated at high-volume centers.
41 ity is strongly associated with prostate and hepatic cancers, whereas reduced CaMKK2 activity has bee