Breast cancer is a common malignancy that arises from cells in the breast, most often in the ducts or lobules. It develops through a multistep process in which genetic mutations and epigenetic changes disrupt normal control of cell growth and division.

A key driver of many breast cancers is hormone signaling. Tumors that express estrogen or progesterone receptors can be stimulated by these hormones, which promote proliferation. Therapies that block hormone production or receptor activity are central to treatment for these hormone receptor positive cancers. Other tumors overexpress HER2, a receptor tyrosine kinase that amplifies growth signaling; targeted drugs against HER2 have significantly improved outcomes.

Genetic predisposition plays a substantial role in some patients. Pathogenic variants in BRCA1, BRCA2 and other susceptibility genes impair DNA repair, increase genomic instability and raise lifetime risk. However, most cases arise from a complex interplay of many low penetrance variants and environmental or lifestyle factors such as reproductive history, obesity, alcohol consumption, and exposure to ionizing radiation.

At the cellular level, the disease is characterized by uncontrolled proliferation, evasion of cell death, angiogenesis, invasion and metastasis. The tumor microenvironment, including immune cells and stromal components, influences progression and response to therapy.

Detection and management rely on imaging, biopsy and molecular characterization. Treatment may combine surgery, radiotherapy, chemotherapy, endocrine therapy, targeted agents and, increasingly, immunotherapy. Research is focusing on tumor heterogeneity, resistance mechanisms, liquid biopsy approaches and more precise risk stratification to tailor screening and treatment and to improve survival while reducing overtreatment.