Breast Cancer

Breast cancer begins in breast tissue. Common invasive forms include invasive ductal carcinoma and invasive lobular carcinoma. Ductal carcinoma in situ (DCIS) remains inside the milk ducts and is not invasive cancer, although it can increase the risk of later invasive disease. Breast cancer can also occur in men.

Clinical care often groups tumors by estrogen receptor (ER), progesterone receptor (PR), and HER2 status. Hormone receptor-positive, HER2-positive, and triple-negative cancers differ in biology, treatment options, and patterns of recurrence.

• A new breast or underarm lump, thickening, or change in texture
• A change in breast size, shape, or contour
• Skin dimpling, peau d'orange, redness, or thickening
• Nipple inversion, a change in nipple position, or non-lactational discharge, especially bloody discharge
• Scaling, ulceration, or persistent eczema-like change of the nipple or areola
• Persistent focal pain
• Rapidly developing redness, swelling, warmth, and skin thickening, which may occur in inflammatory breast cancer

Most breast changes are not cancer, but a new or persistent change should be evaluated by a healthcare professional.

• Increasing age and female sex
• A family history of breast or ovarian cancer
• Inherited variants in BRCA1, BRCA2, PALB2, TP53, PTEN, and other susceptibility genes
• A personal history of breast cancer or selected high-risk breast lesions
• Dense breasts
• Chest radiation at a young age
• Longer lifetime exposure to endogenous estrogen
• Certain menopausal hormone therapy regimens
• Alcohol use
• Postmenopausal overweight or obesity
• Physical inactivity
• Reproductive and breastfeeding factors may influence risk but should never be used to blame a patient

Most people with one or more risk factors will not develop breast cancer, and some people with breast cancer have no obvious risk factor.

• Mammography is the main screening tool for most people at average risk. Starting age and screening interval vary by country, professional organization, and individual risk.
• People at high inherited or familial risk may need earlier screening, breast MRI, genetic counseling, or intensified surveillance.
• Breast self-awareness may help a person notice changes but does not replace evidence-based screening.
• Risk reduction includes limiting alcohol, maintaining a healthy weight, exercising regularly, and obtaining professional genetic counseling when inherited risk is suspected.
• For selected people at high risk, clinicians may discuss risk-reducing medication or surgery after a careful assessment of benefits, harms, and personal values.

Diagnosis is discussed within the Overview, Screening, Staging, and Biomarkers sections above for this cancer type. Specific tests depend on presentation, site, and pathology.

TNM staging combines tumor size and local extent, regional lymph nodes, and distant metastasis.

Breast cancer also uses prognostic stage, which integrates anatomy with grade and ER, PR, and HER2 results.

Histologic grade is commonly reported with the Nottingham system, which evaluates tubule formation, nuclear features, and mitotic activity.

Stage 0 usually refers to in situ disease; stages I–III are local or regional disease; stage IV indicates distant metastasis.

Stage alone does not determine individual prognosis; subtype, treatment response, age, comorbidities, and other factors also matter.

ER- and/or PR-positive tumors use hormone receptor signaling. HER2-positive tumors overexpress HER2 protein or have HER2 gene amplification. Triple-negative breast cancer lacks ER, PR, and HER2 by standard definitions and contains several internal molecular subtypes.

Important pathways include PI3K/AKT, cell-cycle control, DNA repair, and immune evasion. Breast cancer commonly spreads to bone, lung, liver, or brain, although patterns differ by subtype.

• ER and PR
• HER2 by immunohistochemistry and/or in situ hybridization
• Ki-67 as a proliferation marker, interpreted within laboratory and clinical context
• Germline BRCA1/2, PALB2, and other inherited susceptibility genes
• PIK3CA, AKT1, and PTEN alterations in selected advanced HR-positive/HER2-negative disease
• ESR1 mutations associated with acquired endocrine resistance and treatment selection in advanced disease
• PD-L1 in selected triple-negative breast cancers
• Multigene expression assays in selected early HR-positive/HER2-negative cancers
• HER2-low and HER2-ultralow expression categories, which are treatment-related expression groups rather than separate pathologic cancer types

No biomarker should be interpreted in isolation. Assay method, tumor sample, disease stage, and prior treatment can change its clinical meaning.

• HER2
  Human Epidermal Growth Factor Receptor 2
• BRCA1 / BRCA2
  Breast Cancer gene 1 and 2

• Local therapy includes breast-conserving surgery, mastectomy, sentinel lymph-node biopsy or other axillary management, and radiation therapy.
• Systemic therapy may include chemotherapy, endocrine therapy, HER2-directed therapy, CDK4/6 inhibitors, PARP inhibitors, immunotherapy, and antibody-drug conjugates.
• Neoadjuvant treatment can shrink a tumor, test treatment sensitivity, and support surgical planning.
• Adjuvant treatment is used to reduce the risk of recurrence after local therapy.
• Metastatic breast cancer is usually treated with the goals of long-term disease control, symptom relief, and preservation of quality of life.
• Treatment should be individualized by subtype, stage, menopausal status, inherited risk, prior therapies, organ function, and patient preferences.

• Chemotherapy: doxorubicin, epirubicin, cyclophosphamide, paclitaxel, docetaxel, carboplatin, capecitabine, and gemcitabine
• Endocrine therapy: tamoxifen, aromatase inhibitors, fulvestrant, ovarian suppression, and newer estrogen receptor-directed agents
• CDK4/6 inhibitors: abemaciclib, ribociclib, and palbociclib, with different approved settings
• HER2-directed therapy: trastuzumab, pertuzumab, ado-trastuzumab emtansine, fam-trastuzumab deruxtecan, tucatinib, and other approved agents
• PI3K/AKT pathway-directed therapy: alpelisib or capivasertib in defined molecular contexts
• PARP inhibitors: olaparib or talazoparib in selected BRCA-associated settings
• Immunotherapy: pembrolizumab in selected triple-negative breast cancer settings
• Antibody-drug conjugates: sacituzumab govitecan, datopotamab deruxtecan, and other agents according to subtype, prior therapy, and regional approval

• Trastuzumab
  HER2-directed monoclonal antibody · Targeted therapy
• Tamoxifen
  Selective estrogen receptor modulator (SERM) · Hormone therapy

• Surgery: pain, infection, reduced shoulder mobility, lymphedema, and effects on body image or mental health
• Radiation: skin reaction, fatigue, breast swelling, and uncommon late heart or lung effects depending on the treatment field
• Chemotherapy: bone marrow suppression, nausea, hair loss, mucositis, neuropathy, cardiac toxicity, and fertility effects, depending on the regimen
• Endocrine therapy: hot flashes, joint symptoms, bone loss, blood clots, or uterine effects, depending on the drug
• HER2-directed therapy: cardiac monitoring may be needed; selected antibody-drug conjugates can cause interstitial lung disease
• Immunotherapy: immune-related inflammation can affect multiple organs
• Supportive care may include fertility preservation, bone health, exercise rehabilitation, lymphedema services, sexual health care, psychosocial support, nutrition, and pain management.

New shortness of breath, persistent cough, fever, chest pain, severe diarrhea, or neurologic symptoms during treatment should be reported promptly.

• Research is refining the use of CDK4/6 inhibitors in carefully selected high-risk early HR-positive/HER2-negative disease.
• HER2-directed antibody-drug conjugates are being studied across HER2-positive, HER2-low, and HER2-ultralow disease.
• ESR1, PIK3CA, AKT1, PTEN, and inherited DNA-repair genes are increasingly used to guide targeted therapy in advanced disease.
• Circulating tumor DNA is being investigated for molecular residual disease and recurrence monitoring.
• New estrogen receptor degraders and targeted protein degradation approaches are expanding endocrine treatment options.
• De-escalation studies aim to reduce axillary surgery, chemotherapy, or radiation in patients who can safely receive less treatment.
• Recent U.S. regulatory examples include FDA approval of vepdegestrant for ER-positive, HER2-negative, ESR1-mutated advanced or metastatic breast cancer on May 1, 2026; two early-stage HER2-positive indications for fam-trastuzumab deruxtecan on May 15, 2026; and additional triple-negative breast cancer approvals in May and June 2026. These approvals are indication-specific and U.S.-specific.

• What are the exact pathologic type, grade, and stage?
• What are the ER, PR, HER2, and Ki-67 results?
• Should I have germline genetic testing or tumor genomic testing?
• Am I a candidate for breast-conserving surgery, and will I need radiation?
• Should treatment begin before surgery?
• What benefit is expected from chemotherapy, endocrine therapy, HER2-directed therapy, or another targeted treatment?
• Would a multigene expression test be useful in my situation?
• How can we protect my heart, bones, fertility, and lymphatic system?
• Which side effects require an urgent call?
• Are there clinical trials appropriate for my subtype and stage?