In the year 404, Huiyuan wrote a treatise On Why Monks Do Not Bow Down Before Kings (沙門不敬王者論).[4] This book symbolized his efforts to assert the political independence of Buddhist clergy from the courts of monarchic rulers. At the same time, it was a religious and political text that aimed to convince monarchs and Confucian-minded ministers of state that followers of Buddhism were ultimately not subversive. He argued that Buddhists could make good subjects in a kingdom due to their beliefs in retribution of karma and the desire to be reborn in paradise. Despite the Buddhists' reputation of leaving their family behind for a monastic life, Huiyuan stated "those who rejoice in the Way of the Buddha invariably first serve their parents and obey their lords."[1]
p53 is the most commonly mutated tumor suppressor gene in human cancers. In addition to the loss of tumor suppression function and exertion of dominant-negative effects over the remaining wild-type protein, several p53 mutants can gain novel oncogenic functions (gain-of-function, GOF) that actively regulate cancer development and progression. In hu...
To observe whether endothelial cell (EC) progenitors (CD(34)(+)-positive mononuclear cells) participated in neovasculogenesis of ovarian epithelial carcinoma through in vitro and in vivo experiments, and to explore the mechanism of tumor neovasculogenesis. CD(34)(+)-positive mononuclear cells were isolated from peripheral blood of ovarian epithelia...
... Temserolimus was FDA approved for the treatment of advanced renal cell carcinoma in 2007 and is currently being evaluated in several clinical trials for its use in the treatment of gynecologic malignancies, including ovarian carcinoma.[28] Cell culture studies [10,293031 and mouse models323334353637 also suggested that PI3K pathway inhibitors are efficient in suppressing ovarian cancer cell growth. We analyzed the effect of the PI3K, AKT and mTORC1 inhibitors LY294002, SH-6 and rapamycin, respectively, on ovarian cancer cell growth using established cell lines and fresh human tumor tissue. ...
To compare the therapeutic and toxic profile of topotecan given intraperitoneally with intravenously in human ovarian cancer xenografted into athymic nude mice. Eighty female Balb-c/nu-nu mice were randomized assigned into eight groups (n=10). Xenografts resulted from intramesentery injection of cultured human ovarian cancer cells SKOV3 in athymic...
... Previous studies have discovered high IKCal expressions in endometrial carcinoma, breast cancer, urinary bladder carcinoma, colon cancer, and glioblastoma cells. [4][5][6][7] This study demonstrated the close relationship between the Ca 2+ -activated K + channel and cervical cancer. [8,9] This study utilized the K + -channel blocker clotrimazole (CLT) and small hairpin ribonucleic acid (RNA) to explore the role played by (and the effect of) IKCal in the proliferation of HeLa cells. ...
Chemoresistance is the major obstacle to cure endometrial cancer, whereas metformin has demonstrated sensitization to chemotherapy in endometrial cancer. A novel finding states that isocitrate dehydrogenase 1 (IDH1) involves in cancer chemoresistance. Recent studies have revealed that epigenetic modifications facilitate chemoresistance. However, wh...

The purpose of the study was to explore the role and mechanism of ataxia-telangiectasia mutated (ATM) protein in endometrial carcinogenesis. A reverse-phase protein array (RPPA) was used to analyze the expression of ATM signal pathway proteins in Ishikawa and progesterone-insensitive Ishikawa. ATM expression was detected in endometrium specimens by...
To examine the expressions of glyoxalase I (GLO-I) in endometrial cancer tissues and cell lines and to investigate the roles of GLO-I on proliferation and apoptosis in endometrial cancer cells. Immunohistochemistry, western blot and RT-PCR were used to investigate the expressions of GLO-I protein and mRNA in endometrial cancer tissues and Ishikawa...
... Interestingly, estradiol may play a dual role in modulating NRF2 activity. On the one hand, its metabolites activate NRF2 via the generation of reactive oxygen species (ROS) (independent of the ER) [29]. While recent studies demonstrated that estradiol leads to an activation of NRF2 in a wide range of cell types [30,31], the estradiol effect was only noted on protein and not on mRNA levels, suggesting that the main effect of estradiol is based on NRF2 protein stabilization [32]. ...
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