Genomic instability is a characteristic of most cancer cells. It is an increased tendency of genome alteration during cell division. Cancer frequently results from damage to multiple genes controlling cell division and tumor suppressors. It is known that genomic integrity is closely monitored by several surveillance mechanisms, DNA damage checkpoint, DNA repair machinery and mitotic checkpoint. A defect in the regulation of any of these mechanisms often results in genomic instability, which predisposes the cell to malignant transformation. Post-translational modifications of the histone tails are closely associated with regulation of the cell cycle as well as chromatin structure. Nevertheless, DNA methylation status is also related to genomic integrity. We attempt to summarize recent developments in this field and discuss the debate of driving force of tumor initiation and progression.Open access to the scientific literature means the removal of barriers (including price barriers) from accessing scholarly work. There are two parallel roads towards open access: Open Access articles and self-archiving. Open Access articles are immediately, freely available on their Web site, a model mostly funded by charges paid by the author (usually through a research grant). The alternative for a researcher is self-archiving (i.e., to publish in a traditional journal, where only subscribers have immediate access, but to make the article available on their personal and/or institutional Web sites (including so-called repositories or archives)), which is a practice allowed by many scholarly journals.
Open Access raises practical and policy questions for scholars, publishers, funders, and policymakers alike, including what the return on investment is when paying an article processing fee to publish in an Open Access articles, or whether investments into institutional repositories should be made and whether self-archiving should be made mandatory, as contemplated by some funders.
Last date updated on June, 2014