Cancer and Epigenetics

Cancer is a programming problem. Any mechanism that disrupts DNA function may increase risk of carcinogenesis. There was some debate about epigenetic effects causing cancer when I was an NCI Principal Investigator doing cancer research in the 1980s. That debate has now been resolved.

Frequencies can affect any cellular mechanism and I have frequencies for a least five different cellular processes that can be disrupted to help stop tumor growth. I’m always looking for new research on new mechanisms to develop new frequencies.

The Wikipedia has a definition of epigenetics: In biology today, epigenetics has two closely related meanings:

  • The study of the processes involved in the unfolding development of an organism. This includes phenomena such as X chromosome inactivation in mammalian females, and gene silencing within an organism.
  • The study of heritable changes in gene function that occur without a change in the sequence of nuclear DNA. This includes the study of how environmental factors affecting a parent can result in changes in the way genes are expressed in the offspring…

In both cases, the object of study includes how gene regulatory information that is not expressed in DNA sequences is transmitted from one generation (of cells or organisms) to the next – that is (harking back to the Greek prefix), ‘in addition to’ the genetic information encoded in the DNA.

In recent years, there has been rapid progress in understanding epigenetic mechanisms, which include differences in DNA methylation, as well as difference in chromatin structure. Another possibility involves the genomes of cytoplasmic elements (chloroplasts and mitochondria). Other mechanisms have also been proposed. See epigenetic inheritance for a more detailed discussion.

Cancer Epigenetics Enters the Mainstream

Genetics and genomics must share an ever-widening spotlight

By Mark Greener, The Scientist
Volume 19, Issue 12, Page 18, Jun. 20, 2005

The genetic model of cancer – the idea that key mutations lead to unchecked cellular proliferation – has guided cancer research for decades. Thousands of papers report sequence alterations that disrupt, delete, or overexpress genes, leading to oncogenesis. Then, in 1983, Bert Vogelstein and Andrew Feinberg at Johns Hopkins University reported widespread loss of DNA methylation at cytosine-guanine (CpG) dinucleotides in tumor samples. This was the first evidence that eigenetic changes, which are heritable but outside of the genome sequence, might spur cancer. Many remained skeptical, however, regarding the change as an epiphenomenon to primary genetic disruption.

Epigenetics remained the preserve of a few cognoscenti who, away from the spotlight, made steady progress. In the last decade or so, their results have moved to the fore and are helping to unravel the complexities of cancer pathogenesis, raising the prospect of improved diagnosis, more effective prevention, and enhanced treatments. “Epigenetics has entered the mainstream,” Feinberg says. Indeed, epigenetics increasingly shares the research and clinical spotlight with genomics. “Most cancers arise from the interplay of genetic and epigenetic elements,” adds Wolf Reik, from the Babraham Institute, Cambridge, UK. “You can’t study one aspect any more. You have to study both.”

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