Fatty diet during pregnancy may cause cancer in offspring
London: Chemicals or foods that raise estrogen levels during pregnancy may increase cancer risk in daughters, granddaughters, and even great-granddaughters, a new study has claimed.
Pregnant rats on a diet supplemented with synthetic estrogen or with fat, which increases estrogen levels, produce ensuing generations of daughters that appear to be healthy, but harbour a greater than normal risk for mammary cancer.
Although the findings by scientists from Virginia Tech and Georgetown University have not yet been validated in humans, the study shows that environmental damage may be passed from one generation to the next not through genetic mutations, but through “epigenetic” alterations that influence how genomic information is decoded.
The research also raises hope that people who may be especially sensitive to carcinogens can be identified and novel prevention strategies can be employed before cancer strikes.
“We have shown for the first time that altered DNA methylations modulated by specific diet in normal development are heritable and transgenerational,” Yue “Joseph” Wang said.
“We also identified key methylation alteration sites that may be involved or responsible for increased breast cancer risk, which may serve as novel biomarkers for scientists to develop novel and targeted prevention strategies,” Wang said.
According to Leena Hilakivi-Clarke, a professor of oncology at Georgetown Lombardi Comprehensive Cancer Center, two thirds of breast cancers that occur in families have no known genetic cause.
The study shows what may be underlying the cancer are not genetic mutations, but inherited effects of maternal intake of high-fat diets and exposure to excess estrogen during pregnancy.
“It is becoming clear that the process of epigenetic signalling — which genes are expressed and which genes are silenced — is being affected by a mother`s hormonal environment during pregnancy,” Hilakivi-Clarke said.
“The early studies indicate in a normal pregnancy a woman may have more than 20 different estrogen levels, and the highest and the lowest all result in a healthy baby. The challenge has been to understand how something in fetal development can affect breast cancer risk more than 50 years later,” Hilakivi-Clarke said.
The study was led by Sonia de Assis, a postdoctoral researcher in Hilakivi-Clarke`s laboratory at the Georgetown Lombardi Comprehensive Cancer Center at Georgetown University Medical Center.
Virginia Tech researchers developed mathematical models and machine-learning techniques to analyze the changes in DNA methylation status in the descending daughters to understand how increased cancer risk is transmitted without genetic mutation.
DNA methylation is a key process in normal development, allowing cells with the same genome to perform different functions by adding chemical groups to DNA to turn some genes on and some genes off.
Wang’s group found that the descendants with increased risk had several hundred common DNA regions that were methylated differently than in a control group, providing statistically convincing evidence that breast cancer risk can be transmitted via epigenetic means.
“Ultimately, it may be possible to undo or prevent this harmful methylation and decrease the risk of breast cancer,” Wang added.
The study has been recently published in Nature Communications.
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