Epigenetics and cancer

Whoa! Here’s a hypothesis about cancer from some researchers that gives the whole process a significant twist.

A Johns Hopkins researcher, with colleagues in Sweden and at the Fred Hutchinson
Cancer Research Center, suggests that the traditional view of cancer as a group
of diseases with markedly different biological properties arising from a series
of alterations within a cell’s nuclear DNA may have to give way to a more
complicated view. In the January issue of Nature Reviews Genetics, available
online Dec. 21, he and his colleagues suggest that cancers instead begin with
"epigenetic" alterations to stem cells.

 

"We’re not contradicting the view that genetic
changes occur in the development of cancers, but there also are epigenetic
changes and those come first," says lead author Andrew Feinberg, M.D., M.P.H.,
King Fahd Professor of Medicine and director of the Center for Epigenetics in
Common Human Disease at Johns Hopkins.

Feinberg and his colleagues propose that cancers develop via a three-step
process. First, there is an epigenetic disruption of progenitor cells within an
organ or tissue, altered by abnormal regulation of tumor-progenitor genes. This
leads to a population of cells ready to cause new growth.

The second step involves an initiating mutation within the population of
epigenetically disrupted progenitor cells at the earliest stages of new cell
growth, such as the rearrangement of chromosomes in the development of leukemia.
This mutation normally has been considered the first step in cancer development.

The third step is genetic and epigenetic instability, which leads to
increased tumor evolution.

Many of the properties of advanced tumors, including the ability to spread,
or metastasize, are inherent properties of the progenitor cells that give rise
to the primary tumor, Feinberg notes. These properties do not necessarily
require other mutations to occur.

"Greater attention should be paid to the apparently normal cells of patients
with cancer or those at risk for cancer, as they might be crucial targets for
epigenetic alteration and might be an important target for prevention and
screening," he says.

Science rersearch is often good news/bad news. The bad news here is that–if the empigenetic hypothesis is true–it adds another layer of complexity to the process of tumor formation. Just what we need, more complexity! The good news is that this insight is probably really important to understanding and, eventually, dealing with cancer. Nature doesn’t care whether or not reality is convenient.

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