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Comparison of background parenchymal enhancement and fibroglandular density at breast magnetic resonance imaging between BRCA gene mutation carriers and non-carriers

      Highlights

      • BRCA mutation carriers demonstrated lower levels of BPE and amount of FGT tissue than age-matched non-carriers.
      • These differences highlight different risks in distinctive subgroups of breast cancer (hormone-enriched, mutation-associated defective DNA damage repair).
      • Differences in the indications for imaging between the carrier and control groups (screening and breast cancer evaluation, respectively) probably accounted for the higher rate of BI-RADS 3 in the control group.

      Abstract

      Objective

      High background parenchymal enhancement and amount of fibroglandular tissue on breast magnetic resonance imaging are related to increased breast cancer risk. This study sought to compare these parameters between BRCA mutation carriers and non-carriers and to evaluate the potential implications of the findings for short term follow-up. Materials and Methods: Magnetic resonance imaging studies of known BRCA mutation carriers, were compared to age-matched non-carrier studies performed in the same center during the same period. The groups were compared for qualitative background parenchymal enhancement and amount of fibroglandular tissue using the Breast Imaging Reporting and Data System (BI-RADS).

      Results

      Breast parenchymal enhancement was high in up to one-third of the cohort: 22% of carriers and 33% of controls (p = 0.013). These results were sustained on separate analysis of menstrual-cycle-timed examinations. Amount of fibroglandular tissue was high in most cases: 62% of carriers and 75% of controls (p = 0.004). A BI-RADS final assessment score of 3 was more common in patients with high parenchymal enhancement, especially controls.

      Conclusion

      BRCA mutation carriers demonstrated lower levels of breast parenchymal enhancement and amount of fibroglandular tissue than age-matched non-carriers. These differences are probably influenced by hormonal status, as well as highlight different risks in distinctive subgroups of breast cancer (hormone-enriched, mutation-associated defective DNA damage repair), affecting considerations of preventive medical treatment. Differences in the indications for imaging between the carrier and non-carrier groups (screening for mutations and breast cancer evaluation, respectively) probably accounted for the higher rate of BI-RADS 3 in the control group.

      Keywords

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