Breast cancer is not a single disease — it’s a group of biologically different subtypes with distinct behaviors, prognoses, and treatment strategies.
The classification is based on histology (cell type), hormone receptor status, HER2 status, and sometimes gene expression profiles.

Below is a comprehensive breakdown of the main subtypes and how treatments differ.

1. By Histologic (Cell Type) Classification

These describe the cancer’s microscopic appearance:

  • Invasive Ductal Carcinoma (IDC) – ~70–80% of cases; begins in ducts, invades surrounding tissue
  • Invasive Lobular Carcinoma (ILC) – ~10–15%; starts in lobules, often less distinct on imaging
  • Other rare histologies:
    • Tubular carcinoma
    • Mucinous (colloid) carcinoma
    • Medullary carcinoma
    • Papillary carcinoma
    • Metaplastic carcinoma

Treatment: Histologic type matters less for systemic therapy decisions than receptor status, but rare types sometimes have better prognosis and may respond differently to chemo.

2. By Hormone Receptor (HR) & HER2 Status

This is the most clinically relevant classification for guiding therapy.

Subtype ER (Estrogen) PR (Progesterone) HER2 Typical Behavior Main Treatments
HR-positive / HER2-negative + ± – Most common (~70%); slower growing; higher late recurrence risk Endocrine therapy (tamoxifen, aromatase inhibitors), ± chemotherapy if high-risk (based on tumor size, grade, genomic assays like Oncotype DX)
HER2-positive (HR+ or HR–) ± ± + Aggressive but highly responsive to HER2-targeted drugs HER2-targeted therapy (trastuzumab, pertuzumab, T-DM1, trastuzumab deruxtecan) + chemotherapy ± endocrine therapy if HR+
Triple-negative breast cancer (TNBC) – – – ~10–15%; more aggressive; higher early recurrence risk Chemotherapy mainstay; immunotherapy (pembrolizumab) in some settings; PARP inhibitors for BRCA-mutated cases

3. By Molecular/Intrinsic Subtype

Determined by gene expression profiling (e.g., PAM50 test). These correlate with HR/HER2 status but refine prognosis.

Molecular Subtype Typical Clinical Match Prognosis Treatment Nuances
Luminal A HR+, HER2–, low Ki-67 Best prognosis; low recurrence Endocrine therapy ± minimal chemo
Luminal B HR+, HER2– or HER2+, high Ki-67 Higher recurrence risk than Luminal A Endocrine therapy + chemo; HER2 therapy if HER2+
HER2-enriched Often HER2+, HR– Aggressive but HER2-targeted therapy effective HER2-targeted + chemo
Basal-like Often overlaps with TNBC Worst prognosis without treatment Chemo; immunotherapy; targeted agents for BRCA mutations

4. By Stage & Other Special Types

Certain rare but clinically important forms:

  • Inflammatory breast cancer (IBC) – Rapid onset redness/swelling; always stage III+ at diagnosis; needs neoadjuvant chemo, HER2 therapy if positive, then surgery & radiation.
  • Paget’s disease of the nipple – Associated with DCIS or invasive cancer; treated surgically.
  • Metaplastic breast cancer – Rare, chemo-resistant; clinical trial consideration.
  • Male breast cancer – Usually HR+; treated similarly to postmenopausal women.

Treatment Overview by Subtype

Subtype First-Line Systemic Approach Local Therapy Emerging/Targeted Approaches
HR+ / HER2– Endocrine therapy (tamoxifen, AIs, ± ovarian suppression in premenopause); chemo if high risk Surgery + radiation depending on stage CDK4/6 inhibitors, PI3K inhibitors (alpelisib) for PIK3CA-mutant
HER2+ Chemo + trastuzumab ± pertuzumab Surgery + radiation T-DM1, trastuzumab deruxtecan, tucatinib in advanced disease
TNBC Chemo ± immunotherapy (pembrolizumab in PD-L1+ or early high-risk) Surgery + radiation PARP inhibitors (BRCA-mutant), antibody-drug conjugates (sacituzumab govitecan)
IBC Neoadjuvant chemo ± HER2 therapy Modified radical mastectomy + radiation Immunotherapy trials
Metastatic Depends on receptor status Palliative radiation for local control Multiple targeted/novel agents in clinical trials

Key takeaway:

  • Receptor status (ER/PR/HER2) drives most systemic treatment choices.
  • Histology gives insight into growth patterns and prognosis but less directly affects systemic therapy.
  • Molecular profiling increasingly personalizes care, helping avoid overtreatment or undertreatment.

Breast Cancer Subtype & Treatment Pathway Chart

Subtype Key Features Typical First-Line Systemic Treatment Local Treatment Targeted/Emerging Therapies
HR+ / HER2–(Luminal A & Luminal B) ER+, PR+, HER2–; most common; slower growth in Luminal A, faster in Luminal B Endocrine therapy (Tamoxifen, Aromatase Inhibitors ± ovarian suppression); Chemo if high-risk (Oncotype DX/Prosigna guided) Surgery + radiation if indicated CDK4/6 inhibitors (palbociclib, ribociclib, abemaciclib); PI3K inhibitors (alpelisib for PIK3CA mutation)
HER2+ (HR+ or HR–) HER2 overexpressed; more aggressive without therapy Chemo + HER2-targeted therapy (trastuzumab ± pertuzumab) Surgery + radiation T-DM1, trastuzumab deruxtecan, tucatinib (advanced/metastatic)
Triple-Negative (TNBC)(Basal-like) ER–, PR–, HER2–; more aggressive; higher early recurrence risk Chemo (anthracyclines, taxanes, platinum) ± immunotherapy (pembrolizumab for PD-L1+) Surgery + radiation PARP inhibitors (olaparib, talazoparib for BRCA-mutant); sacituzumab govitecan; clinical trials
Inflammatory Breast Cancer (IBC) Rapid swelling/redness; always ≥ stage III Neoadjuvant chemo ± HER2 therapy if HER2+ Modified radical mastectomy + radiation Immunotherapy & targeted therapy trials
Metaplastic Breast Cancer Rare; chemo-resistant Standard chemo Surgery + radiation Clinical trials, targeted agents in research
Male Breast Cancer Usually HR+ Endocrine therapy; surgery Surgery ± radiation Same targeted therapies as postmenopausal women with same receptor status
Paget’s Disease of Nipple Eczematoid nipple lesion; often with DCIS/invasive Depends on underlying tumor subtype Surgery (often mastectomy) ± radiation Guided by receptor status