In the United States, 10 to 20 percent of women with breast cancer or ovarian cancer have a first- or second-degree relative with one of these diseases. Men with breast cancer have an even higher likelihood. The familial tendency to develop these cancers is called hereditary breast–ovarian cancer syndrome. The best known of these, the "BRCA" mutations, confer a lifetime risk of breast cancer of between 60 and 85 percent and a lifetime risk of ovarian cancer of between 15 and 40 percent. Some mutations associated with cancer, such as "p53", "BRCA1" and "BRCA2", occur in mechanisms to correct errors in DNA. These mutations are either inherited or acquired after birth. Presumably, they allow further mutations, which allow uncontrolled division, lack of attachment, and metastasis to distant organs. However, there is strong evidence of residual risk variation that goes well beyond hereditary "BRCA" gene mutations between carrier families. This is caused by unobserved risk factors. This implicates environmental and other causes as triggers for breast cancers. The inherited mutation in "BRCA1" or "BRCA2" genes can interfere with repair of DNA cross links and DNA double strand breaks (known functions of the encoded protein). These carcinogens cause DNA damage such as DNA cross links and double strand breaks that often require repairs by pathways containing BRCA1 and BRCA2. However, mutations in "BRCA" genes account for only 2 to 3 percent of all breast cancers. Levin "et al." say that cancer may not be inevitable for all carriers of "BRCA1" and "BRCA2" mutations. About half of hereditary breast–ovarian cancer syndromes involve unknown genes. Furthermore, certain latent viruses, may decrease the expression of the "BRCA1" gene and increase the risk of breast tumors.