The attaching of methyl--or chemical--groups onto DNA sequences within the tumor suppressing gene Rb2/p130 can cause the gene to cease functioning in non-small lung cancer cells (NSLC) and retinoblastoma cells, researchers at Temple University’s Sbarro Institute for Cancer Research and Molecular Medicine and Italy’s University of Siena have discovered. Their findings are reported in two studies: “Tumor-specific exon 1 mutations could be the ‘hit event’ predisposing Rb2/p130 gene to epigenetic silencing in lung cancer” and “Genetic and epigenetic alterations of RB2/p130 tumor suppressor gene in human sporadic retinoblastoma: implications for pathogenesis and therapeutic approach,” both of which appear in September issues of Oncogene (www.nature.com/onc).The joint studies at Temple and Siena were coordinated by Antonio Giordano, M.D., Ph.D., director of Sbarro Institute at Temple (www.shro.org), and by Marcella Macaluso of the Sbarro Institute and Caterina Cinti of both Centro Nazionale Ricerche and the University of Siena.
