Benefits of Prophylactic Surgery Vary in BRCA Women

A new study is the first to suggest that the prophylactic removal of the ovaries and fallopian tubes may provide different benefits for women who carry genetic mutations.

The study by researchers from Memorial Sloan-Kettering Cancer Center (MSKCC, New York, NY, USA) followed 886 women over the age of 30 who carry the BRCA1 or BRCA2 genetic mutation. Of this group, 561 opted to have their ovaries and fallopian tubes surgically removed--a procedure called risk-reducing salpingo-oophorectomy--while 325 chose to participate in ovarian surveillance. The women were followed for 40 months via a questionnaire or medical review.

The results showed that overall the prophylactic surgery reduced the incidence of ovarian and related cancers by 89% and decreased breast cancer incidence by 47%. When broken down further, the results indicate that none of the women carrying the BRCA2 mutation who had the surgery developed ovarian cancer, while women carrying the BRCA1 mutation who had the surgery decreased their risk of developing ovarian or related cancers by 87%. The study additionally showed that women with BRCA2 mutations also reduced their risk of developing breast cancer by 72%, while those with BRCA1 mutations reduced their risk of breast cancer by 39%. Why the results of the procedure differ in BRCA1 carriers and BRCA2 is currently unknown. The results were presented at the annual meeting of the American Society of Clinical Oncology, held during June 2006 in Atlanta (GA, USA).

"These findings will help doctors to better counsel women who have an inherited predisposition to ovarian and breast cancers and allow tailoring of risk-reduction strategies depending on what particular mutation a woman has inherited, said lead author Noah D. Kauff, M.D., a gynecologist and geneticist at MSKCC.

BRCA1 and BRCA2 are breast cancer susceptibility genes that were first identified in 1994. People carrying mutated genes are at an increased risk of breast, ovarian, and prostate cancer. The normal gene plays a role in repairing breaks in DNA; however, when the gene is mutated it is thought that this repair function may become disabled, thus leading to more DNA replication errors and cancerous growth.



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Memorial Sloan-Kettering Cancer Center