Epigenetics is a conceptually and practically challenging research area. But research over the past five years has shown that there may be many remaining questions about how cancer arises, spreads, and recurs. Almost 20 years after the human genome was first sequenced in 2003, there are still many open questions about how the genome works. Sequencing the human genome has provided tremendous insight into how our cells and bodies function, but a clearer understanding of the genetic mechanisms underlying many common diseases and health is lacking.
One reason is that while DNA encodes the information that enables cells and tissues
to develop, grow, and repair, gene expression is controlled by other mechanisms.
For our genes to be expressed, they must first be read or transcribed, and then
the molecules they encode must be created or translated.
For the cellular machinery to be able to read the DNA, it must be able to access
the DNA itself. Many mechanisms influence this, but it is becoming increasingly
clear that the way DNA is wrapped around proteins called histones and packaged into
fibers known as chromatin plays a key role.
Professor Trevor Graham, Professor of Genomics and Evolution at the Institute for
Cancer Research (ICR) in London, said in an interview with Medical News: “The logic
is that if DNA is completely entangled and trapped in a large chunk of the genome,
those genes are inaccessible for machines to extract and may be turned off.”, genes
may be expressed if they are in an uncharacterized region of DNA," he explained.
This is a form of epigenetic regulation, as gene expression is not due to changes
in the DNA sequence but other processes that affect its accessibility.
Historically, cancer
is viewed as the result of an accumulation of mutations within cells. A
major focus has been on environmental causes of cancer mutations
that increase the risk of developing certain types of cancer.
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