Disruption Of Cell Cycle Arrest Research Articles

Epigenetics Meets Radiation Biology as a New Approach in Cancer Treatment

Cancer is a disease that results from both genetic and epigenetic changes. In recent decades, a number of people have investigated the disparities in gene expression resulting from variable DNA methylation alteration and chromatin structure modification in response to the environment. Especially, colon cancer is a great model system for investigating the epigenetic mechanism for aberrant gene expression alteration. Ionizing radiation (IR) could affect a variety of processes within exposed cells and, in particular, cause changes in gene expression, disruption of cell cycle arrest, and apoptotic cell death. Even though there is growing evidence on the importance of epigenetics and biological processes induced by radiation exposure in various cancer types including colon cancer, specific epigenetic alterations induced by radiation at the molecular level are incompletely defined. This review focuses on discussing possible IR-mediated changes of DNA methylation and histone modification in cancer.

Trapping the mouse genome to hunt human alterations

Glioblastoma multiforme (GBM) are the most common and aggressive adult primary brain tumors. Genetic alterations and their consequences in these malignant astrocytomas have been studied extensively and include (i) overexpression of growth factors and their corresponding receptors (fibroblast growth factor, epidermal growth factor, and platelet-derived growth factors), (ii) abnormalities of transduction signaling pathways (activation of PI3 kinase/AKT, RAS/MAP kinase, and protein kinase C), or (iii) disruption of cell cycle arrest (loss of p16INK4A and p14ARF, mutations in p53 protein, and PTEN) (1). Whether these modifications are causative or participate in tumor progression is a pivotal question that can best be answered by modeling glioma formation in mice. In this issue of PNAS, Kamnasaran et al. (2) combine genetically engineered murine (GEM) models of gliomas with a retroviral gene-trapping approach to identify new molecular alterations in human gliomas.