Gene performance identified as key factor in breast cancer treatment

GENES linked to fat metabolism could help doctors identify women at greater risk of specific types of breast cancer.

Genetic activity indicates whether women are likely to develop a hormone-sensitive cancer, affecting treatment – as drugs can only treat breast cancer if they are fuelled by the female sex hormone oestrogen.

Study leader Seema Khan, from Northwestern University in Chicago, said: “Currently three drugs can be used to prevent breast cancer in women who are at extremely high risk for the disease.

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“However, these drugs prevent only breast cancers that are sensitive to hormones, commonly referred to as oestrogen receptor-positive breast cancers. They do not prevent breast cancers that are insensitive to hormones, or oestrogen receptor-negative breast cancers.

“We should not expose women at risk for hormone-insensitive breast cancer to the side effects of preventive medications that we know will not work for them.”

The scientists studied fine-needle biopsy samples from the unaffected breasts of 15 women with hormone-sensitive breast cancer, and the same number of women with tumours that were unresponsive to oestrogen.

After validating their results in a second group of women, they identified 13 genes with significantly higher activity levels in hormone-insensitive samples.

Eight of these genes were associated with the metabolism, or breakdown, of fats.

“This was interesting because obesity is a breast cancer risk factor for post-menopausal women, but obese women are generally thought to be at increased risk for hormone-sensitive cancer,” said Dr Khan.

She added: “It will be a few more steps before this information is practically useful, but we are hoping that it can take us to a place where we can obtain a breast sample from healthy women, see that they are at risk for a certain type of breast cancer and tailor the prevention strategy accordingly.”

The findings were published in the journal Cancer Prevention Research this week.