Abstract
Abstract BACKGROUND: Cervical cancer (CC) is the second most prevalent neoplasia in women and fifth cause of death by cancer in this population worldwide. Pap smear and HPV infection test have been the most widely used tools to detect cytological abnormalities and women's risk of developing cancer. However, they cannot distinguish between lesions that will progress to an invasive carcinoma and those that will not. Methylation biomarkers could be useful in early detection and progression for cervical carcinoma. Thus, the aim of this study was evaluate the promoter methylation status of a selected gene as possible biomarker for early detection and progression of cervical carcinogenesis in women in the South of Chile. METHODS: DNA isolated from 12 normal samples and 7 cervical cancers was enriched with Methylated DNA Immunoprecipitation (MeDIP) and hybridized to Nimblegen 385K CpG Islands plus Promoter arrays. Bioinformatics strategies were used for background correction, array normalization and data analysis of differentially methylated genomic regions between tumor and normal tissue. The promoter methylation status of selected gene was validated by Methylation Specific PCR (MSP) in biopsies samples of the cervix: 44 normal, 22 Low Grade Lesions (LSIL), 22 High Grade Lesions (HSIL) and 45 cervical cancers (CC). The associations between methylation status of selected gene and different stages of progression of cervical cancer were analyzed using a Chi-square test. FINDINGS: SPRP4 gene was selected from microarray as potential biomarker, because it showed a high score of methylation in cancer, according to bioinformatic analysis. The methylation frequency of SPRP4 through MSP was 0% in normal samples, 50% in LSIL, 27% in HSIL and 100% in tumor samples. Thus, promoter methylation of SPRP4 was associated to cervical cancer and related lesions (p<0.05). INTERPRETATION: The promoter methylation status of SFRP4 has potential use as a biomarker for diagnosis of cervical cancer. Therefore, the validation of this marker in a case-control cohort is warranted. FUNDING: National Cancer Institute grant U01-CA84986; Oncomethylome Sciences, SA, Comisión Nacional de Ciencia y Tecnología (CONICYT; Chile, Becas Chile; Conicyt No24090095; CORFO 07CN13PBT-222). Postdoctoral Fondecyt Research Project 3120141. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 5575. doi:1538-7445.AM2012-5575
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