Breast cancer is the most frequently diagnosed malignancy in women in the United States. Triple receptor-negative breast cancer (TNBC) represents a small percentage of all breast cancers, but it constitutes the majority of breast cancers of the basal-like subtype. TNBC is characterized by the lack of expression of estrogen and progesterone receptors and by the lack of overexpression of human epidermal growth factor receptor-2 (HER2). Published studies have shown that TNBC is highly sensitive to chemotherapy in the neoadjuvant, adjuvant, and metastatic settings. Even with TNBC’s high sensitivity to chemotherapy, patients with TNBC have high recurrence and relapse rates. Many of the ongoing clinical trials available for patients with TNBC focus on the safety and/or efficacy of new, targeted agents given alone or in combination with standard or alternative chemotherapy.
Breast cancer is the number one malignancy diagnosed in women in the United States. In 2009, it was estimated that more than 190,000 individuals would be diagnosed with breast cancer and approximately 40,000 would die from the disease.1
The incidence of invasive breast cancer has decreased over the years, largely because screening rates have increased, facilitating earlier diagnosis. Even when diagnosed early, however, triple receptor–negative breast cancer (TNBC) has a poor prognosis and represents a major unmet need.
Molecular Subtypes of Breast Cancer
Breast cancer consists of a group of diseases with many clinical, pathologic, and molecular characteristics that affect prognosis and treatment. There are 4 intrinsic breast cancer subtypes by gene expression: basal-like, HER2, luminal A, and luminal B.2
These 4 subtypes have been shown to have different prognoses and different responses to therapy.2-5
Clinical Characteristics of Triple Receptor–Negative Breast Cancer (TNBC)
TNBC represents about 10% to 15% of all breast cancers and constitutes more than 80% of all basal-like diagnoses.7-9
TNBC’s classification is established by the lack of ER and PR expression by immunohistochemical (IHC) assay and by the normal expression of HER2 by IHC or fluorescence in situ hybridization.
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