Children who eat fries raise their risk of breast cancer later in life

November 18, 2017

The U.S. researchers say that in a study of American nurses they found that one additional serving of fries per week, at ages three to five, increased breast cancer risk by 27 percent.

Study leader, Dr. Karin Michels, of Brigham and Women's Hospital in Boston and Harvard Medical School, says that research is finding more evidence that diet early in life could play a role in the development of diseases in women later in life.

She says this study provides additional evidence that breast cancer may originate during the early phases of a woman's life, and that eating habits during that phase may be particularly important to reduce future risk of breast cancer.

In their study, Michels and colleagues used an ongoing survey of female registered nurses, and looked at 582 women with breast cancer and 1,569 women free of breast cancer in 1993.

The researchers looked at the women's diets and at questionnaires filled out by the mothers of the participants.

They say that one risk factor for breast cancer stood out, women whose mothers who said their daughters ate french fries, had a higher risk of breast cancer, and this risk increased 27 percent for each weekly serving reportedly eaten.

Michels does say however that as the data was dependent on the validity of the maternal recall of the diet the results must be interpreted cautiously.

She says that as mothers were asked to recall their daughter's preschool diet after the participants' breast cancer status was known, it is possible that mothers of women with breast cancer recalled their daughter's diet differently than mothers of healthy women.

Apparently other foods perceived as less healthy, such as hot dogs or ice cream, were not associated with breast cancer risk.

Previous research has also linked a high-fat diet with breast cancer.

Breast cancer affects more than 200,000 U.S. women a year and is expected to kill 40,000 this year.

The study is published in the International Journal of Cancer.

The researchers first applied a test that could tell them whether the offending gene was "upstream" or "downstream" from activated FANCD2 -- that is, did action of the mutant gene fall in the molecular pathway before FANCD2 was activated, or after, respectively? The answer was that the problem was located downstream from a normally functioning FANCD2.

The researchers then mapped SNPs in the genome of those patients and families, looking for changes in which a single chemical building block in the DNA differs from the usual building block at that position. Because FA is a recessive genetic disease, an affected child needs to inherit two copies of an errant gene, each from a parent that carried a single mutation.

They were startled to find only one suspect location in the entire genome, on chromosome 17, that was present in all four families. Further research uncovered two candidate genes within that region, and none of the patients had an abnormality in one of them. But they all had mutations in the second gene, BRIP1.

"What was very surprisingly to us is that while all five patients were homozygous for a mutation in the gene, as expected, all had the same mutation in this gene," Auerbach says. In other words, the five patients each inherited two copies of the same mutation, one from each parent.

When the researchers looked at the other families in their registry with no known mutations in any of the genes associated with the disease, they found six more patients with this same BRIP1 mutation, three of whom were homozygous.

Now the story began to make sense to the researchers, since the protein, BACH1, produced by BRIP1, was known to be a DNA helicase, a class of enzymes which unwind the two strands of the DNA double helix so that DNA synthesis can take place. And they knew from the scientific literature that BACH1 interacts with BRCA1 protein.

"This is the first gene associated with Fanconi anemia that we have a defined function for," says Auerbach. "It interacts directly with BRCA1, and is known to play a role in the repair of DNA double-strand breaks."

BACH1 could be the link between FANCD2 and BRCA1, the researchers say.

"It may be that DNA can't be repaired without a normally functioning BACH1," says Auerbach. "So perhaps FANCD2 activation isn't the endpoint, as had been thought, but that it has to do something downstream that can't be accomplished if BACH1 is not present."