“We already know that some of the things people can do to help prevent cancer with certain dietary approaches or lifestyle,” said Dashwood. “Now we hope to better understand the molecular processes in progress, even in epigenetics. This should open the door to new approaches to disease prevention or treatment through diet, and to complement conventional drug therapies.”According to Rod Dashwood, a professor of environmental toxicology and molecular Leader Chemoprotection LPI cancer, epigenetics is a unifying theory, in which many health problems ranging from cancer to cardiovascular disease and neurological disorders may be caused at least partially abnormal “changes of histones, “and their effects on the reading of DNA in cells.
In studies on cancer, heart disease, neurological disorders and other degenerative diseases, scientists are moving away from the “nature and nurture” debate and find that you’re not a creature is genetic or environmental, but two – with enormous implications for a new approach to health.
OSU scientists recently received a $ 8.5 million grant from the National Cancer Institute to explore these issues, making the LPI program one of the leaders in the nation on diet, epigenetics, and cancer prevention. The positive results of laboratory research have already converted placebo-controlled human intervention on health problems such as colon and prostate cancer, which are among the most common cancers in the United States.
OSU scientists have published a series of studies on these topics in journals such as cancer research, research for cancer prevention, carcinogenesis, and seminars in the field of cancer biology. Among the more recent discoveries is that the organoselenium compounds naturally present in foods could prevent the progress of human prostate and colon through a mechanism of inhibition of HDAC.
Some of the more recent work in this area has been described by researchers at the Linus Pauling Institute at Oregon State University, speaking at Experimental Biology 2010, a business conference in Anaheim, California
In the case of cancer, tumor suppressor genes can cause cancer cells to die by acting as a brake on the uncontrolled growth of cells. But too HDAC enzyme can “turn off” tumor suppressor genes, although the DNA sequence at the base of the cell – its genetic structure – has not been altered or transferred. If this happens, the cells continue to reproduce without control, which is a fundamental characteristic of cancer development.
The new field of “epigenetics” is rapidly revealing how people, plants and animals begin with a certain genetic code at conception. But the choice of which genes are “expressed” or activated, is strongly influenced by environmental factors. Gene expression may change rapidly over time, can be influenced by external factors, these changes can be transmitted to offspring, and can literally the key to life and death.
“We believe that many diseases that have aberrant expression of the gene to their roots can be linked to how DNA is packaged, and actions of enzymes such as histone deacetylases, or HDACs,” Dashwood said. “Not later than 10 years ago we knew almost nothing about the interruption of HDAC in cancer or other diseases, but is now one of the most promising areas of health research.”
“Some therapeutic drugs already used for cancer treatment in a clinical setting will probably work, at least in part, because they act as HDAC inhibitors,” said Dashwood. “And what is most intriguing is that HDAC inhibition may affect many degenerative health problems, not just cancer. Heart disease, stroke, bipolar disorder, and even aging may have ties with altered HDAC / histone.
The good news – for cancer and perhaps many other health problems – is that “HDAC inhibitors” can stop this degenerative process, and some of them have already been identified in foods are common examples. sulforaphane in broccoli, indole-3-carbinol in cruciferous vegetables, and organic compounds in vegetables such as garlic and onion. butyrate, a compound produced in the intestine when dietary fiber is fermented, is an HDAC inhibitor, and provides a possible explanation for why higher intake of dietary fiber may help prevent cancer.
“Metabolism seems to be a key factor, even the generation of HDAC active site of action,” said Dashwood. “In cancer cells, p21 tumor suppressors such as p53 and often become epigenetically silence. HDAC inhibitors can help you turn, makeup and cancer cells to commit suicide by apoptosis.
“In the future, an HDAC inhibitor may be only conceptually the benefits to more than a problem of degenerative diseases.”