How the epigenetics of cancer may yield clues to treatment
It’s a question that lurks in the minds of so many cancer patients—even those too dignified or gracious to express it out loud: “Why me?” For those unfortunate enough to face a cancer recurrence, a second question may surface: Why do some patients, following treatment, continue on cancer-free for the rest of their lives while others wind up battling the disease again and, possibly, again? What causes some patients to have a significantly poorer prognosis than others?
Nita Ahuja: “In some people the cause of cancer
might simply be abad genetic code. In others,
it’s because epigenetic events have caused
many genes to stop functioning normally.”
It’s one of many questions that have fueled genetic research for decades now. Armed with an answer, oncologists could potentially solve a problem that has proved equally perplexing: how to differentiate between patients who definitely need chemotherapy and those for whom the treatment is superfluous and not worth the risk.
As geneticists and researchers continue to pursue a better understanding of the relationship between human genes and illness, that question is slowly being answered. For surgical oncologist Nita Ahuja, the answer lies in the study of epigenetics: events that affect or change a gene’s expression or signature.
While some aspects of our genetic makeup are inalterable, concrete and permanently etched into our DNA, epigenetic studies probe how genes can be turned off by circumstances such as diet and environment. In some patients, Ahuja says, the explanation for a poor prognosis might be found in genes that have, at some point, been turned off epigenetically, interrupting the natural sequence of things—their signature or expression. Patients whose genes have not experienced such an event may have a good prognosis, or more specifically, a lower risk of cancer recurrence. Those who have the “bad” genes may be less fortunate. The latter, she says, would merit chemotherapy.
What causes these genes to lose their normal function is often linked to an epigenetic event called DNA methylation, a process (launched, for instance, by excessive exposure to a toxin) that causes a chemical alteration in gene expression and disrupts the natural pathway of that gene. As a result, Ahuja explains, that patient might be more at risk for a cancer relapse.
“Epigenetic occurrences are a more common cause of cancer,” Ahuja says, “because diet and chemical exposures might cause so many gene manipulations over the course of a lifetime.”
If physicians could determine whether certain individuals exhibit the kinds of genetic malfunctions, so to speak, that would cause them to have a poorer prognosis, treatment could be vastly improved.
Those patients, she says, would more likely benefit from chemotherapy, while in other patients, chemotherapy might be overkill. To that end, a primary focus of Ahuja’s study—which involves primarily colon cancer—includes the possibility of a test that could differentiate between those patients. Ahuja and her colleagues are also testing whether epigenetic therapy can turn on the function of such genes and be used in treatment of colorectal cancers.
“If we could potentially identify these patients through the use of epigenetic markers,” Ahuja says,“this would be incredibly personalized medicine.”
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