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RISS 인기검색어
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- 저자 : Rui-Lan Huang (검색결과 2 건)
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HOCl Oxidation-modified CT26 Cell Vaccine Inhibits Colon Tumor Growth in a Mouse Model
Zhou, Rui,Huang, Wen-Jun,Ma, Cong,Zhou, Yan,Yao, Yu-Qin,Wang, Yu-Xi,Gou, Lan-Tu,Yi, Chen,Yang, Jin-Liang Asian Pacific Journal of Cancer Prevention 2012 Asian Pacific journal of cancer prevention Vol.13 No.8
Despite progress in elucidating mechanisms associated with colorectal cancer and improvement of treatment methods, it remains a frequent cause of death worldwide. New and more effective therapies are therefore urgently needed. Recent studies have shown that immunogenicity of whole ovarian tumor cells and subsequent T cell response were potentiated by oxidation modification with hypochlorous acid (HOCl) in vitro and ex vivo. These results prompted us to investigate the protective antitumor response with an HOCl treated CT26 colorectal cancer cell vaccine in an in vivo mouse model. Administration of HOCl modified vaccine triggered robust antitumor immunity to autologous tumor cells in mice and prolonged survival period significantly. In addition, increased necrosis and apoptosis were found in tumor tissue from the oxidation group. Interestingly, ELISPOT assays showed that specific T cell responses were not elicited in response to the immunizing cellular antigen, in contrast to raising sera antibody titer and antibody binding activity shown by ELISA assay and flow cytometry. Further evaluation of the mechanisms underlying HOCl modified vaccine mediated humoral immunity highlighted the role of antibody-dependent cell-mediated cytotoxicity. These results combined with previous studies suggest that HOCl oxidation modified whole cell vaccine has wide applicability as a cancer vaccine because it can target both T cell- and B cell-specific responses. It may thus represent a promising approach for the immunotherapy of colorectal cancer.
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Genotypespecific methylation of HPV in cervical intraepithelial neoplasia
Yaw-Wen Hsu,Rui-Lan Huang,Po-Hsuan Su,Yu-Chih Chen,Hui-Chen Wang,Chi-Chun Liao,Hung-Cheng Lai 대한부인종양학회 2017 Journal of Gynecologic Oncology Vol.28 No.4
Objective: Hypermethylation of human papillomavirus (HPV) and host genes has beenreported in cervical cancer. However, the degree of methylation of different HPV typesrelative to the severity of the cervical lesions remains controversial. Studies of the degree ofmethylation associated with the host gene and the HPV genome to the severity of cervicallesions are rare. We examined the association of methylation status between host genes andlate gene 1 (L1) regions of HPV16, 18, 52, and 58 in cervical brushings. Methods: Cervical brushings from 147 HPV-infected patients were obtained. The samplescomprised normal (n=28), cervical intraepithelial neoplasia (CIN) 1 (n=45), CIN2 (n=13), andCIN3/carcinoma in situ (n=61). The methylation status of HPV and host genes was measuredusing bisulfite pyrosequencing and quantitative methylation-specific polymerase chainreaction (PCR). Results: The degree of methylation of L1 in HPV16, 18, and 52 was associated with theseverity of the cervical lesion. In HPV52, C-phosphate-G (CpG) sites 6368m, 6405m, and6443m showed significantly higher methylation in lesions ≥CIN3 (p=0.005, 0.003, and0.026, respectively). Methylation of most HPV types except HPV52 (r<−0.1) was positivelycorrelated with the degree of methylation of host genes including PAX1 and SOX1 (0.4≤r≤0.7). Combining HPV methylation with PAX1 methylation improved the clustering for ≥CIN2. Conclusion: Our study showed that the degree of L1 methylation of HPV16, 18, and 52but not 58 is associated with the severity of cervical lesions. The association betweenHPV methylation and host gene methylation suggests different responses of host cellularepigenetic machinery to different HPV genotypes.
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