From the results of the first part of this project, it can be concluded that the familial aggregation of BC in the family is probably not explained by a single high-risk mutation but rather by two or more variants that each has low to moderate effects on BC risk.
Út frá niðurstöðunum má álykta að há tíðni BK í fjölskyldunni sem skoðuð var í fyrri hluta verkefnisins skýrist trúlega ekki af stakri stökkbreytingu sem ber með sér mikla áhættuaukningu.