Combination chemotherapy regimen provided the most benefit for triple-negative breast cancer

Cyclophosphamide, methotrexate and 5-FU chemotherapy produced the greatest magnitude of benefit for patients with triple-negative breast cancer, results from International Breast Cancer Study Group trials VIII and IX showed.

“Recognition of factors predictive of response has become crucial for understanding treatment effects in the adjuvant treatment of breast cancer,” researchers wrote. “We demonstrated that the magnitude of the effect of chemotherapy in early breast cancer significantly correlates with tumor subtypes identified by immuohistochemistry.”

The researchers analyzed 2,257 patients for whom immunohistochemical-defined tumor subtype was available — about 82% of the total cohort in trials VIII and IX. Three hundred and three patients (13%) had triple-negative breast cancer; 119 (5%) had HER-2–positive, endocrine receptor-absent disease; and 1,835 (81%) had HER-2–positive, endocrine receptor-present disease.

Roughly half of the cohort, 56%, was assigned to cyclophosphamide, methotrexate and 5-FU chemotherapy.

After a median follow-up of 11 years, cumulative incidence rates showed that 21% of triple-negative patients assigned chemotherapy relapsed compared with 36% of those who did not undergo chemotherapy. Patients with HER-2–positive, endocrine receptor-absent disease who underwent chemotherapy saw a similar benefit, 27% vs. 41% in those who did not undergo chemotherapy.

Researchers said the magnitude of chemotherapy effect was low for patients with HER-2–positive, endocrine receptor-absent and endocrine receptor-present disease. In contrast, chemotherapy was associated with a significant reduction in risk for patients with the triple-negative subtype (HR=0.46; 95% CI, 0.29-0.73) when compared with the endocrine receptor-present subtype.

Researchers also noted a smaller effect for patients with endocrine receptor-absent disease when compared with the endocrine receptor-present subtype (HR=0.58; 95% CI, 0.29-1.17).

Colleoni M. J Clin Oncol. 2010;doi:10.1200/JCO.2009.25.9549.