Breast cancer arises when cells in breast tissue acquire genetic and epigenetic changes that disrupt normal growth control, leading to uncontrolled proliferation, local invasion and sometimes metastasis. It is a heterogeneous disease comprising several biological subtypes with distinct behaviors and treatment responses. Key molecular classifications include hormone receptor positive, HER2 positive and triple negative breast cancers. These subtypes are defined by expression of estrogen and progesterone receptors, overexpression or amplification of the HER2 gene, or lack of all three markers.

Risk factors involve a combination of inherited and environmental influences. Inherited mutations in genes such as BRCA1 and BRCA2 substantially increase lifetime risk by impairing DNA repair pathways. Other important contributors include reproductive history, hormone exposure, obesity, alcohol intake and age. Early detection through imaging and pathological assessment improves outcomes, but accurate subtyping at the molecular level has become equally critical for guiding therapy.

Current treatments combine surgery, radiotherapy, cytotoxic chemotherapy, endocrine therapy and targeted agents. Endocrine therapies block estrogen signaling in hormone receptor positive disease. HER2 targeted therapies inhibit HER2 signaling and have transformed outcomes for HER2 positive tumors. For triple negative breast cancer, options remain more limited, though chemotherapy, immunotherapy and agents targeting DNA repair defects are used.

Ongoing research focuses on understanding tumor heterogeneity, the tumor microenvironment and mechanisms of resistance. Genomic and transcriptomic profiling are being used to refine classification and identify novel targets. Immunotherapies, PARP inhibitors for tumors with DNA repair defects and combinations of targeted drugs aim to improve survival while reducing toxicity. Early detection, risk stratification and personalized treatment remain central goals in breast cancer research.