The 4 Main Molecular Subtypes of Breast Cancer*
| Type | Expression | Characteristics | Prognosis | Therapy |
| Luminal A | HR+/HER2− | Slow-growing, less aggressive than other subtypes | Favorable prognosis, particularly in short term | Antihormone therapy |
| Luminal B | HR+/HER2+ | Highly positive for Ki-67 (indicator of large proportion of actively dividing cells) or HER2; tends to be higher-grade | Poorer survival than for luminal A cancers | Chemotherapy, hormone therapy, and treatments targeting HER2 receptor |
| Triple-negative | HR−/HER2− (ER−, PR−, and HER2−) | Twice as common in black women as in white women in United States; more common in premenopausal women and those with BRCA1 gene mutation | Poorer short-term prognosis than for other subtypes | No current targeted therapy |
| HER2-enriched | HR−/HER2+ | Grows and spreads more aggressively than other subtypes | Poorer short-term prognosis than for HR+ breast cancers; recent widespread use of targeted therapies for HER2+ cancers has improved outcomes | Combination of surgery, radiation therapy, chemotherapy, or targeted therapy such as the immune monoclonal antibody trastuzumab |
*The different subtypes differ in risk factors, presentation, response to treatment, and outcome. Techniques to profile tumor gene expression allow better understanding of subtypes but are costly and complex. Subtypes are approximated using biologic markers, including presence or absence of ER or PR and excess levels of HER2 or extra copies of HER2 gene (HER2+/HER2−) (5,48).