Breast Cancer: An Overview
What breast is, how common it is, how it's found, and how diagnosis and treatment are guided.
What it is
Breast cancer is a malignant proliferation of cells arising in the tissues of the breast, most often in the epithelial cells lining the ducts and lobules. It is not a single disease but a family of disorders that differ in how the cells look under the microscope, how they behave, and which molecular signals drive their growth. At one end of the spectrum sit in situ lesions, in which abnormal cells remain confined within the duct or lobule; at the other sit invasive carcinomas, which have breached that boundary and can spread to lymph nodes and distant organs. Understanding which type a person has is the foundation of everything that follows in diagnosis and management.
How common it is
Breast cancer is the most commonly diagnosed cancer in women and the second most common cancer diagnosis overall. For 2026, roughly 321,910 new invasive cases are projected among women in the United States, alongside about 60,730 cases of ductal carcinoma in situ (DCIS); men account for far fewer, with about 2,670 projected cases [1]. The age-adjusted incidence is approximately 132.5 new cases per 100,000 women per year (2019, 2023) [2]. Over a lifetime, a woman in the United States has roughly a 13% chance, about 1 in 8, of being diagnosed [2].
The trend is an active area of attention. Incidence has been rising by about 1% per year over the past decade, and the increase is steeper, roughly 1.4% per year, among women under 50 [1]. The reasons are not fully settled and are the subject of ongoing investigation.
Who is at risk factors fall into two broad groups: those a person cannot change and those that are modifiable.
Non-modifiable factors. Age is among the strongest: the median age at diagnosis is about 63, and risk rises as women get older [1]. Female sex itself is the dominant factor, with women accounting for more than 99% of cases [1]. Inherited (germline) pathogenic variants, most notably in BRCA1 and BRCA2, but also others, substantially raise lifetime risk and can inform risk-reducing strategies [1]. A first-degree family history of breast cancer and a history of high-dose chest radiation before age 30 also increase risk, as do high mammographic breast density and certain benign but proliferative lesions such as atypical hyperplasia or prior DCIS/LCIS [1].
Modifiable factors. Reproductive and hormonal influences include early menarche or late menopause, never having children or a first child after age 30, and use of combined menopausal hormone therapy [1]. Lifestyle factors include excess body weight (particularly after menopause), alcohol consumption, and physical inactivity [1]. The evidence suggests these factors shift risk at the population level; they do not determine any individual's outcome, and many people diagnosed have no identifiable risk factor at all.
How it is found
Most breast cancers today are detected through screening, before any symptoms appear. The principal screening modality is mammography, including digital mammography and tomosynthesis (3-D mammography). Breast MRI is used as a supplemental tool for women at high risk, and ultrasound can serve as an adjunct in selected situations [3].
Guidance on screening differs among expert bodies, and start age and interval remain contested. The US Preventive Services Task Force (2024) recommends biennial screening mammography for women at average risk between ages 40 and 74 [3]. The American Cancer Society offers annual options beginning at age 45, with the choice to start as early as 40, and notes that women at high risk may begin earlier and incorporate MRI [1]. Supplemental screening for women with dense breasts is an evolving area. This overview describes these positions neutrally and is not a recommendation to any individual reader; screening decisions are best made with a clinician who knows the person's full history.
When breast cancer is symptomatic rather than screen-detected, the most common presentation is a palpable mass. Other presentations include skin or nipple changes and nipple discharge [3].
Outlook
Survival statistics for breast cancer are, on the whole, encouraging, and they have improved markedly over time. Death rates fell by approximately 44% from 1989 through 2022, a decline attributed to earlier detection and better treatment [1]. The overall 5-year relative survival is about 91% [2].
Survival varies substantially by how far the cancer has spread at diagnosis. Based on SEER data (2016, 2022), 5-year relative survival is approximately [2]:
- Localized (confined to the breast): ~99%
- Regional (spread to nearby lymph nodes/structures): ~86%
- Distant (spread to distant organs): ~32%
These are population figures, not individual predictions. They describe the average experience of large groups of people diagnosed years ago and cannot tell any single person what will happen to them. An individual's outlook depends on tumor biology, molecular subtype, treatment response, overall health, and factors not captured in these summary numbers, and the figures predate some of the most recent therapeutic advances. They are best read as orientation, not prophecy.
A bridge to diagnosis and classification
Once cancer is suspected, the diagnosis is confirmed and classified on tissue, where the pathologist distinguishes in situ from invasive disease and assigns a histologic type, from the common invasive carcinoma of no special type and invasive lobular carcinoma to special subtypes such as tubular, mucinous, metaplastic, and rarer entities including adenoid cystic and secretory carcinoma, the last of which is defined molecularly by a recurrent ETV6-NTRK3 fusion that also confers eligibility for TRK-targeted therapy [14]. This morphologic classification, combined with tumor grade and the extent of spread (stage), establishes the framework on which all subsequent decisions rest.
A bridge to how treatment is guided
Beyond morphology, a panel of biomarkers refines the picture and links each tumor to specific therapy classes: estrogen and progesterone receptors (ER/PR) [4], HER2 (ERBB2) status [5], and the Ki-67 proliferation index [6], supplemented in selected cases by gene-expression assays such as the 21-gene recurrence score [7] and 70-gene signature [8]. Additional biomarkers, including germline BRCA1/BRCA2 [9], PIK3CA [10] and acquired ESR1 [11] mutations, PD-L1 [12], mismatch-repair/MSI status with tumor mutational burden [13], and NTRK fusions [14], identify eligibility for particular drug classes. None of this constitutes treatment advice for any individual; it is the scientific basis on which a multidisciplinary team and patient make decisions together.
References
- Siegel RL, Kratzer TB, Wagle NS, Sung H, Jemal A. Cancer statistics, 2026. CA Cancer J Clin. 2026. doi:10.3322/caac.70043.
- National Cancer Institute. SEER Cancer Stat Facts (SEER*Explorer); 2026 release (2019, 2023 incidence; 2020, 2024 mortality; 2016, 2022 survival). seer.cancer.gov/statfacts.
- US Preventive Services Task Force. Breast Cancer: Screening (2024 Recommendation). uspreventiveservicestaskforce.org; 2024.
- Allison KH, Hammond MEH, Dowsett M, et al. Estrogen and Progesterone Receptor Testing in Breast Cancer: ASCO/CAP Guideline Update. Arch Pathol Lab Med / J Clin Oncol. 2020. PMID 31928354. doi:10.1200/JCO.19.02309.
- Wolff AC, Somerfield MR, Dowsett M, et al. Human Epidermal Growth Factor Receptor 2 Testing in Breast Cancer: ASCO/CAP Guideline Update. Arch Pathol Lab Med / J Clin Oncol. 2023. PMID 37303228. doi:10.1200/JCO.22.02864. Modi S, Jacot W, Yamashita T, et al. Trastuzumab Deruxtecan in HER2-Low Advanced Breast Cancer (DESTINY-Breast04). N Engl J Med. 2022. PMID 35665782. doi:10.1056/NEJMoa2202914.
- Johnston SRD, Harbeck N, Hegg R, et al. Abemaciclib Combined With Endocrine Therapy for High-Risk Early Breast Cancer (monarchE). J Clin Oncol. 2020. PMID 32954927. doi:10.1200/JCO.20.02514. Harbeck N, Rastogi P, Martin M, et al. Adjuvant abemaciclib combined with endocrine therapy: monarchE Ki-67 analysis. Ann Oncol. 2021. PMID 34656740. doi:10.1016/j.annonc.2021.09.015.
- Paik S, Shak S, Tang G, et al. A Multigene Assay to Predict Recurrence of Tamoxifen-Treated, Node-Negative Breast Cancer. N Engl J Med. 2004. PMID 15591335. doi:10.1056/NEJMoa041588. Sparano JA, Gray RJ, Makower DF, et al. Adjuvant Chemotherapy Guided by a 21-Gene Expression Assay (TAILORx). N Engl J Med. 2018. PMID 29860917. doi:10.1056/NEJMoa1804710.
- Cardoso F, van't Veer LJ, Bogaerts J, et al. 70-Gene Signature as an Aid to Treatment Decisions in Early-Stage Breast Cancer (MINDACT). N Engl J Med. 2016. PMID 27557300. doi:10.1056/NEJMoa1602253.
- Robson M, Im SA, Senkus E, et al. Olaparib for Metastatic Breast Cancer in Patients with a Germline BRCA Mutation (OlympiAD). N Engl J Med. 2017. PMID 28578601. doi:10.1056/NEJMoa1706450. Tutt ANJ, Garber JE, Kaufman B, et al. Adjuvant Olaparib for Patients with BRCA1- or BRCA2-Mutated Breast Cancer (OlympiA). N Engl J Med. 2021. PMID 34081848. doi:10.1056/NEJMoa2105215.
- André F, Ciruelos E, Rubovszky G, et al. Alpelisib for PIK3CA-Mutated, Hormone Receptor-Positive Advanced Breast Cancer (SOLAR-1). N Engl J Med. 2019. PMID 31091374. doi:10.1056/NEJMoa1813904. Turner NC, Oliveira M, Howell SJ, et al. Capivasertib in Hormone Receptor-Positive Advanced Breast Cancer (CAPItello-291). N Engl J Med. 2023. PMID 37256976. doi:10.1056/NEJMoa2214861.
- Bidard FC, Kaklamani VG, Neven P, et al. Elacestrant versus Standard Endocrine Therapy for ER-Positive, HER2-Negative Advanced Breast Cancer (EMERALD). J Clin Oncol. 2022. PMID 35584336. Toy W, Shen Y, Won H, et al. ESR1 ligand-binding domain mutations in hormone-resistant breast cancer. Nat Genet. 2013. PMID 24185512.
- Cortes J, Cescon DW, Rugo HS, et al. Pembrolizumab plus Chemotherapy versus Placebo plus Chemotherapy for Previously Untreated Locally Recurrent Inoperable or Metastatic Triple-Negative Breast Cancer (KEYNOTE-355). Lancet. 2020. PMID 33278935. doi:10.1016/S0140-6736(20)32531-9.
- Marabelle A, Fakih M, Lopez J, et al. Association of Tumour Mutational Burden with Outcomes in Patients with Advanced Solid Tumours Treated with Pembrolizumab (KEYNOTE-158). Lancet Oncol. 2020. PMID 32919526. doi:10.1016/S1470-2045(20)30445-9.
- Drilon A, Li G, Dogan S, et al. What hides behind the MASC: identification of a novel ETV6-NTRK3 fusion in secretory carcinoma. Cancer Discov. 2017. PMID 28183697. doi:10.1158/2159-8290.CD-16-1237. Drilon A, Laetsch TW, Kummar S, et al. Efficacy of Larotrectinib in TRK Fusion-Positive Cancers. N Engl J Med. 2018. PMID 29466156. doi:10.1056/NEJMoa1714448. Doebele RC, Drilon A, Paz-Ares L, et al. Entrectinib in patients with advanced or metastatic NTRK fusion-positive solid tumours. Lancet Oncol. 2020. PMID 31838007. doi:10.1016/S1470-2045(19)30691-6.
