دانلود کتاب درمان سرطان اپی ژنتیک

Epigenetics has come a long way from its earliest incarnations. But how do we now define this phenomenon? The classical definition coined by Waddington in 1942 used a phrase “epigenetic landscape” to describe how genes might interact with their surroundings to produce a phenotype [1,2]. Commonly used definitions nowadays posit epigenetics as a “stably heritable phenotype resulting from changes in a chromosome without alterations in the DNA sequence” [3], or as “chromatin- based events that regulate DNA-templated processes” [4]. A consensus definition still remains elusive. Critically, it is now well established that aberrant epigenetics are a common feature in cancer [5]. There are currently four well-described mechanisms that underpin epigenetic regulation. They are: DNA CpG methylation, histone posttranslational modifications (PTMs), histone variants, and noncoding RNA (ncRNA) [6]. However, the issue of ncRNA being a true epigenetic mechanism is controversial. For example, the journal Clinical Epigenetics describes the issue as “Differential RNA expression levels (coding or non-coding) or RNA modifications cannot be considered as part of epigenetics, and this includes levels of the RNA modifying enzymes or readers,” with associated strict criteria for publication [7]. All four work individually or together to elicit what is often described as the “Epigenetic code.” Generally speaking, this is described as the “epigenome,” and large research programs have been undertaken (e.g., the ENCODE Project Consortium) to generate epigenetic “roadmaps” or “blueprints” of human health and disease including cancer [8]. Given the scale of advances in the field of epigenetics in recent years, this revised volume has been re-designed to reflect these advances and has been restructured accordingly.