The RAD51C is a gene involved in the repair of DNA damage, and pathogenic variants (disease-causing) increase the risk for hereditary breast and ovarian cancer, particularly high-grade serous ovarian cancer. Individuals with a single pathogenic variant have elevated lifetime risks for ovarian cancer and, to a lesser extent, breast cancer. Management focuses on enhanced surveillance and preventive strategies, including consideration of risk-reducing salpingo-oophorectomy (removal of the ovaries and fallopian tubes) and individualized breast screening with MRI depending on personal and family history. RAD51C pathogenic variants are not known to be more common in the Ashkenazi Jewish population.
HBOC due to the RAD51C gene exhibits autosomal dominant inheritance. This means there is a 50% chance the condition can be passed from generation-to-generation. First degree relatives (parents, siblings, children) have a 50% chance to have the same pathogenic variant whereas second degree relatives (grandparents, aunts/uncles, nieces/nephews, half-siblings) have a 25% chance. More distant relatives have lower chances of having the same pathogenic variant when one is identified in the family.
In addition, when an individual inherits pathogenic variants in both copies of the RAD51C gene, it can cause a rare childhood-onset condition called Fanconi anemia. People with this condition may have bone marrow failure, physical abnormalities, organ defects, and an increased risk of certain cancers. Fanconi anemia exhibits autosomal recessive inheritance. This means that both parents must be have a RAD51C pathogenic variant to have a 25% chance to have a child with the condition.
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Written December 2025
