Breast Lumps

A hyperplastic response of both stromal and epithelial components rather than a true neoplasm — essentially an aberration of normal development. Oestrogen is the key driver: they're most common in young women (15–35), enlarge in pregnancy, and tend to involute after menopause.

Cysts arise from the TDLU as part of fibrocystic change, which is so common it's considered an aberration of involution rather than a disease. During the normal cyclical hormonal stimulation, lobular acini undergo repeated proliferation and apoptosis. With progressive involution (typically ages 35–55), there's a mismatch between lobular epithelial secretion and resorption — ducts can become obstructed by periductal fibrosis or stromal involution while the epithelium continues secreting. The acini dilate, forming microcysts that coalesce into macrocysts. The lining can be either flattened atrophic epithelium or apocrine metaplasia (large pink cells with abundant cytoplasm). Apocrine epithelium actively secretes into the cyst, producing the characteristic straw-coloured or dark-green fluid. Cysts are oestrogen-driven and essentially disappear post-menopause without HRT.

Fat necrosis is a sterile inflammatory response to damaged adipocytes, most commonly from trauma (including surgical/biopsy sites) or radiotherapy.

Normal → Usual ductal hyperplasia → Atypical ductal hyperplasia (ADH) → DCIS → Invasive ductal carcinoma

Initiating mutations: Loss of tumour suppressors (TP53, BRCA1/2, RB1) or gain-of-function oncogenes (PIK3CA, HER2/ERBB2 amplification). BRCA1/2 germline mutations impair homologous recombination DNA repair, leading to genomic instability.

Molecular subtypes reflect the cell of origin and dominant pathway: Luminal A/B (ER+, driven by hormonal signalling), HER2-enriched (ERBB2 amplification driving RAS-MAPK and PI3K-AKT proliferative pathways), and triple-negative/basal-like (often TP53/BRCA1-related, high genomic instability).

The transition from in-situ to invasive disease involves breakdown of the myoepithelial cell layer and basement membrane, mediated by matrix metalloproteinases (MMPs), loss of E-cadherin (particularly in lobular carcinoma), and epithelial-to-mesenchymal transition (EMT). The tumour microenvironment — cancer-associated fibroblasts, tumour-associated macrophages, angiogenesis via VEGF — actively facilitates invasion and metastasis.

Types: Ductal Carcinoma Lobular Carcinoma Special Breast Cancer Subtypes Molecular Subtypes of Breast Cancer Phyllodes Tumour