Table 2.
Summary of the breast tumor molecular subtypes.
| Subtype | Alias | Biomarker status | Grade | Outcome | Additional features | PrevalenceΔ | |
|---|---|---|---|---|---|---|---|
| Luminal | Luminal A* | [ER+|PR+]HER2-KI67- | 1|2 | Good | Luminal cytokeratin+, FOXA1+, ADH1B high; cell-cell adhesion genes high | 23.7%[9] | |
| Luminal B* | [ER+|PR+]HER2-KI67+ | 2|3 | Intermediate | Luminal cytokeratin+; TP53-; FGFR1 and ZIC3 amp; ADH1B low; cell-cell adhesion genes high | 38.8%[9] | ||
| [ER+|PR+]HER2+KI67+ | |Poor | 14%[9] | |||||
| HER2 positive | HER2 over-expression* | ER-PR-HER2+ | 2|3 | Poor | TP53-; GRB7 high; cell-cell adhesion genes high | 11.2%[9] | |
| Triple negative | Basal* | ER-PR-HER2-, basal marker+ | 3 | Poor | BRCA1-, TP53-; CDKN2A high; RB1 low; FGFR2 amp; cell-cell adhesion genes high | 10-25%[128] | 12.3%[9] |
| Claudin-low | ER-PR-HER2-, EMT marker+, Stem-cell marker+, claudin- | 3 | Poor | GATA3-regulated genes, cell-cell adhesion genes low; CDH1 low; Claudins low | 7-14%[141] | ||
| Metaplastic breast cancer (MBC) | ER-PR-HER2-, EMT marker+, Stem-cell marker+ | 3 | Poor | GATA3-regulated genes, cell-cell adhesion genes low; PIK3CA-, AKT- or KRAS- | 1%[143] | ||
| Interferon-rich | ER-PR-HER2-, interferon regulated genes+ | 3 | Intermediate | STAT1, SP110 high | ~10%[93] | ||
| Molecular apocrine cancer (MAC) | Molecular apocrine cancer (MAC) | ER-PR-AR+ | 2|3 | Poor | KI67+ | 13.2%[98] | |
* Subtypes with detailed expression patterns and clinical implications discussed in the text, which take the majority of the breast tumor cases and are most commonly referred to.
Δ The percentages could not be added up, as triple negative tumor subtypes are not mutually exclusive and the percentages are taken from different publications.
Δ The prevalences shown here are for all breast tumor cases, which are taken from one particular publication (as indicated in the square brackets) and can vary by different studies.