Students will practice looking at a topic from multiple points of view, and will discuss whose voices are amplified and whose voices are silenced. This lesson is part of a media unit curated at our Digital Citizenship website called "Who Am I Online?".
It is necessary for transformed residual cancer cells to acquire the ability to replicate limitlessly and invade adjacent tissues for recurrence. Therefore, we selected genes that are involved in limitless replicative potential (p14, p15, and p16) and tissue invasion or metastasis (CDH1, integrin α4, and SYK) for this study. Hypermethylation of p16, a cyclin-dependent kinase inhibitor gene that regulates the cell cycle, has been frequently detected in hepatocellular carcinomas (5-7). The p15 gene, another cyclin-dependent kinase inhibitor that is adjacent to p16 on chromosome 9p21, is also aberrantly methylated in hepatocellular carcinoma. The p14ARF antagonizes the murine double minute 2-mediated ubiquitination and degradation of p53 and facilitates p53-mediated cell cycle arrest and apoptosis (8). CDH1 (E-cadherin) mediates homotypic cell-cell adhesion of epithelial cells (9), and promoter methylation of E-cadherin was found in hepatocellular carcinoma (6). Glutathione S-transferases are a family of isoenzymes that play an important role in protecting cells against damage mediated by carcinogens and exogenous drugs by catalyzing the conjugation of glutathione with electrophilic compounds. Many groups have also reported that GSTP1 is transcriptionally silenced by promoter hypermethylation in hepatocellular carcinoma (5, 10, 11). The spleen tyrosine kinase (SYK) gene is a tumor or metastasis suppressor gene that was recently found to be silenced through DNA methylation in breast cancer (12), T-lineage acute lymphoblastic leukemia (13), and hepatocellular carcinoma (14). 2b1af7f3a8