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J Cancer Res Ther ; 2019 Apr; 15(2): 426-436
Article | IMSEAR | ID: sea-213636

Résumé

Aims and Methods: Retrospectively, this paper compared the differences of the Epstein–Barr virus (EBV)-encoded small RNAs (EBERs), protein expression and gene mutations of tumor suppressor gene p53 (TP53) in keratinized nasopharyngeal squamous cell carcinoma (KNSCC) and nonKNSCC, and the relationships between pathological features and the prognosis of patients were analyzed. Results: The positive rate of EBERs hybridization and TP53 expressions was 76.3% and 52.2%, respectively, while the mutation rate of TP53 gene was 39.6%. Logistic regression analysis showed direct relationships between the subtypes of nasopharyngeal squamous cell carcinoma (NPSCC) and EBERs-positive, or frequent consumption of pickled food. Overall survival rates of patients with positive TP53 expression, the TP53 gene mutations, vascular invasions, organ metastases, lymph node metastasis, and clinical recurrence were significantly lower than those of patients without those symptoms. The poorer prognosis was related to regularly drinking and the advanced age. According to the Cox regression analysis, we found that the main prognostic factors of NPSCC patients were the aging, recurrence, TP53 gene mutations, especially exon 7 or 8 mutations. Conclusions: We concluded that there were the correlations between NPSCC subtypes with EBV infection and frequent intaking of pickled food, while aging, clinical recurrence, and TP53 gene mutations were independent predictors for the poor prognosis of nasopharyngeal carcinoma

2.
Article Dans Anglais | IMSEAR | ID: sea-135039

Résumé

Background: Vitamin E is a potent growth inhibitor of various cancer cell types in vitro and in vivo. The cell death mechanism is believed to be via cell cycle blockage, differentiation, and apoptosis. Objectives: To determine the possible involvement of protein expression of MEK-2 and ERK-2 in the cell death mechanism induced by palm oil ?-tocotrienol and ?-tocopherol in human cervical cancer cell line, CaSki cells. Methods: In this study, we tested the effect of ?-tocotrienol and ?-tocopherol on the proliferation and apoptosis in CaSki cells. Western blot analysis was used to determine the involvement of MEK-2 and ERK-2 in regulating the cell death mechanism. Results: Gamma-tocotrienol and α-tocopherol efficiently inhibited the proliferation of CaSki cells by 85.2% to 90.8% (p<0.01, n=4) and 10.2% to 39.1% (p<0.01, n=4) beginning at 100 μM and 50 μM, respectively. The possible cell death mechanism induced by both compounds may be due to apoptosis as confirmed by the presence of cellular DNA fragments separated by electrophoresis and enhancement of apoptotic activity. Treatment with γ-tocotrienol at 150 μM markedly decreased the protein expression of MEK-2 and ERK-2 at 12 hours and 18 hours. In contrast, treatment with α-tocopherol at 300μM has no effect on both protein expressions. Conclusion: The transient decreases in the protein expression of MEK-2 and ERK-2 suggested that the anti proliferative effect of γ-tocotrienol might involve alteration of the proliferative signaling cascade.

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