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  • American Association for Cancer Research (AACR)  (4)
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  • American Association for Cancer Research (AACR)  (4)
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  • 1
    Online Resource
    Online Resource
    American Association for Cancer Research (AACR) ; 2013
    In:  Cancer Research Vol. 73, No. 3_Supplement ( 2013-02-01), p. C5-C5
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 73, No. 3_Supplement ( 2013-02-01), p. C5-C5
    Abstract: Esophageal squamous cell carcinoma (ESCC) is the sixth leading cause of cancer death among men in Taiwan, and the five-year survival rate is below 10%. The retinoic acid receptor beta2 (RAR-beta2) is frequently deleted or silenced at early stages in tumor progression. Most of RAR-beta2 repressions was associated with promoter hypermethylation in several epithelial carcinomas. The aim of this study is to investigate RAR-beta2 promoter methylation status in different stages of ESCC patients. Through methylation-specific PCR analysis, methylation rate of RAR-beta2 was 21.1% (15/71) in tumor cases, but unmethylated in all normal counterparts. In RAR-beta2 promoter hypermethylation cases, the methylation frequency of lymph nodes invasion and tumor metastasis was twofold increased. Moreover, RAR-beta2 promoter methylation frequency was increased with 14.7% and showed significant decrease survival rate in advanced stage. Esophageal cancer cell lines 81T, 81T 1-1 and 81T 1-4 were treated with 5-aza-dC (DNA methylation inhibitor), the level of RAR-beta2 methylation was decreased in all ESCC cell lines. Moreover, migration ability was inhibited in 81T cell line. The migration ability of 81T 1-1 and 81T 1-4 cell lines were decreased about 50%. Our findings indicate that RAR-beta2 hypermethylation in ESCC could be useful for prognosis marker. RAR-beta2 methylation may become one of the clinical therapy targets and invasion-migration markers. Citation Format: Ruei-Siang Wu, Chun-Chieh Yu, Yue-Yuah Li, Ming-Tsang Wu, Ruei-Nian Li. Study of the relationship between RAR-beta2 hypermethylation and invasive esophageal squamous cell carcinoma. [abstract]. In: Proceedings of the AACR Special Conference on Tumor Invasion and Metastasis; Jan 20-23, 2013; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2013;73(3 Suppl):Abstract nr C5.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    RVK:
    RVK:
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2013
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 2
    Online Resource
    Online Resource
    American Association for Cancer Research (AACR) ; 2005
    In:  Cancer Epidemiology, Biomarkers & Prevention Vol. 14, No. 11 ( 2005-11-01), p. 2544-2549
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 14, No. 11 ( 2005-11-01), p. 2544-2549
    Abstract: Human papillomavirus (HPV) infection is a high-risk factor for cervical intraepithelial neoplasm (CIN) but the association between the quantitative HPV DNA load and the severity of CIN remains controversial. We conducted a community study to investigate the correlation between the two. Potential study subjects were selected through Pap smear screening in Kaohsiung County, Taiwan. Ninety-one subjects with either their first case of inflammation or ≥CIN1 by biopsy confirmation were assigned to a case group; 175 normal subjects with negative findings by Pap smears or biopsies were assigned to a control group. Cervical HPV load was detected with Hybrid Capture II assay for high-risk HPV infection, with nested PCR for high- and low-risk HPV infection, and with type-specific PCR for HPV type 16 (HPV-16). Individuals with positive high-risk HPV infection had an increased risk of developing CIN. Compared with HPV-negative subjects, the odds ratios were 32.2 [95% confidence interval (95% CI), 10.4-99.5] for subjects with CIN1, 37.2 (95% CI, 7.4-187.6) for subjects with CIN2, and 68.3 (95% CI, 14.1-328.5) for subjects with ≥CIN3 after adjusting for other confounding factors. The similar trend was also found among the HPV-16–negative individuals. In addition, high-risk HPV DNA load levels were highly correlated with the different grades of CINs in the overall population (Spearman's correlation coefficient r = 0.67, P & lt; 0.0001, n = 266) and the HPV-16–negative population (Spearman's correlation coefficient r = 0.58, P & lt; 0.0001, n = 234). We concluded that high-risk HPV infection, irrespective of HPV-16 infection, was highly and positively associated with the development of CIN.
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2005
    detail.hit.zdb_id: 2036781-8
    detail.hit.zdb_id: 1153420-5
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  • 3
    Online Resource
    Online Resource
    American Association for Cancer Research (AACR) ; 2013
    In:  Cancer Research Vol. 73, No. 3_Supplement ( 2013-02-01), p. B98-B98
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 73, No. 3_Supplement ( 2013-02-01), p. B98-B98
    Abstract: Cervical cancer is one of the most common cancer among women. Early detection and prompt treatment would be the best management options. DNA methylation is one of the epigenetic regulation mechanisms leading to gene silencing in neoplastic cells. Silencing of tumor suppressor gene resulted from aberrant methylation has been detected in a majority of human cancers. Here, we applied methylation-specific polymerase chain reaction (MSP) to examine the methylation state of three tumor suppressor genes (rar-beta, p16 and cdh1) and an inflammatory-related cox-2 gene in different stages of cervical intraepithelial neoplasia (CIN). Our analyses revealed that cox-2 gene is in unmethylated form from CIN I to carcinoma specimens. Besides, no significant increase in methylation levels of rar-beta and cdh1 genes was observed. However, the high frequency of aberrant hypermethylation of p16 gene (13.2% in normal specimens ; 18.2% in CIN I; 35.7% in CIN II; 31.6% in CIN III and 15.4% in carcinoma) suggesting that p16 is progressively increased during the development of malignant stages in cervical intraepithelial neoplasia, especially in the absence of HPV infection. The result of bisulfite sequencing indicated that the 10 CpG sites of p16 gene are all methylated in ten individuals. In conclusion, this study identifies promoter methylation analysis of p16 on cervical cell specimens may be an additional tool for current cervical cytomorphology based screening. Citation Format: Sheng Hsiung Lin, Chun Chieh Yu, Ming Tsang Wu, Ruei Nian Li. Promoter methylation status of tumor suppressor genes and an inflammatory-related COX-2 gene in cervical intraepithelial neoplasia. [abstract]. In: Proceedings of the AACR Special Conference on Tumor Invasion and Metastasis; Jan 20-23, 2013; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2013;73(3 Suppl):Abstract nr B98.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    RVK:
    RVK:
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2013
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
    Location Call Number Limitation Availability
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  • 4
    Online Resource
    Online Resource
    American Association for Cancer Research (AACR) ; 2013
    In:  Cancer Research Vol. 73, No. 3_Supplement ( 2013-02-01), p. C12-C12
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 73, No. 3_Supplement ( 2013-02-01), p. C12-C12
    Abstract: Esophageal cancer ranks as the sixth most deadly cancer and esophageal squamous cell carcinoma (ESCC) is the sixth most common cause of cancer deaths in males in worldwide. Therefore, it is important to identify molecular markers for clinical diagnosis. Homeodomain-only protein X (HOPX)-β is a tumor suppressor gene and its promoter methylation is shown to be frequent in human cancer. Mucin 1 (MUC1) is a transmembrane mucin that is highly expressed in various cancers and correlates with malignant potential. In addition, the degree of whole genome methylation decreases as the lesion progressing from a benign proliferation of cells to an invasive cancer. The aim of this study was to investigate HOPX-β and MUC1 promoter methylation status and global methylation level in different stages of ESCC patients. Methylation-specific PCR (MSP) revealed that the methylation rate of HOPX-β was 26.5% (27/102) in tumor samples and only 9% (9/100) in paired non-tumor samples (p & lt;0.05). In HOPX-β promoter hypermethylation samples, the frequency of lymph node invasion and tumor metastasis was increased about 3-fold and 2-fold, respectively. Furthermore, HOPX-β promoter methylation frequency was increased about 3-fold in advanced stage. On the other hand, the methylation frequency of MUC1 was 90.7% (97/107) in paired non-tumor samples while the methylation frequency was decreased to 53.3% (57/107) in tumor samples. 78.5% (84/107) of tumor samples showed significantly decline in the degree of methylation compared with paired non-tumor samples (p & lt;0.0001). We found a decrease tendency in methylation frequency of MUC1 correlated with clinical stage (early/advanced), the frequency of lymph node invasion and metastasis. Importantly, the methylation rate of MUC1 was inversely related with the tumor size (p=0.0105). The level of global long interspersed nuclear element 1 (LINE-1) methylation in ESCC tissues (mean 65.8%) was significantly lower than paired non-tumor samples (mean 79.5%). However, there is no relation between the level of global LINE-1 methylation and tumor stage or survival rate. Our findings indicate that LINE-1, MUC1 methylation level and HOPX-β hypermethylation in ESCC are useful markers in clinical diagnosis. Citation Format: Yu Chun Kao, Sheng Hsiung Lin, Chun Chieh Yu, Ruei Nian Li, Ming Tsang Wu. Aberrant promoter methylation of HOPX-β, MUC1 genes and global methylation in esophageal squamous cell carcinoma. [abstract]. In: Proceedings of the AACR Special Conference on Tumor Invasion and Metastasis; Jan 20-23, 2013; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2013;73(3 Suppl):Abstract nr C12.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    RVK:
    RVK:
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2013
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
    Location Call Number Limitation Availability
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