Breast Risk Lesions, Mastitis & Male Breast Cancer

Benign epithelial lesions and cancer risk

Why tiers matter. Benign biopsies are graded by the risk of later invasive carcinoma; the added risk from proliferative lesions and atypia applies to both breasts.

Fibrocystic change. The most common benign finding in women of reproductive age, causing cyclic, bilateral tenderness and lumpiness. It combines cysts (blue-domed and fluid-filled), apocrine metaplasia (pink cells with apical snouts) and stromal fibrosis, and it does not raise cancer risk. A simple cyst collapses when aspirated.

Proliferative disease without atypia. Usual ductal hyperplasia fills ducts with a mixed, streaming cell population and irregular slit-like spaces. Sclerosing adenosis crowds compressed acini into dense stroma and often calcifies. A radial scar has a fibroelastic core with ducts radiating outward and appears as a spiculated, stellate density. Both sclerosing adenosis and radial scar imitate invasive carcinoma, but their glands keep a myoepithelial layer (p63, calponin), which invasive carcinoma lacks.

Atypical hyperplasia. Atypical ductal hyperplasia consists of monotonous cells resembling low-grade DCIS but too limited in extent; atypical lobular hyperplasia consists of LCIS-like cells that only partly fill a lobule. Either raises risk about 4–5-fold, prompting enhanced screening and chemoprevention with tamoxifen, raloxifene or an aromatase inhibitor. Atypical ductal hyperplasia on core biopsy is usually excised because carcinoma is sometimes found nearby.

Lobular carcinoma in situ

Pathology. Loss of E-cadherin (CDH1) leaves small, uniform, discohesive cells, sometimes signet-ring cells with intracytoplasmic mucin, filling and distending lobular acini. LCIS forms no mass and usually does not calcify, so it is found incidentally; it is often multicentric and bilateral and is ER-positive.

Significance. Classic LCIS raises the risk of invasive carcinoma, ductal or lobular, roughly 8–10-fold in either breast. Because it is chiefly a risk marker, it is managed with surveillance and chemoprevention (tamoxifen) rather than mastectomy. DCIS differs: its cells are cohesive and keep E-cadherin, it often presents as mammographic microcalcifications, and its risk falls mainly on the same breast.

Inflammatory and reactive lesions

Lactational mastitis. In the first weeks to months after delivery, milk stasis and nipple fissures allow S. aureus (including MRSA) to enter, producing a painful, warm, red, wedge-shaped area with fever and malaise. Nursing or pumping should continue (the milk is safe; abrupt weaning raises abscess risk) with dicloxacillin or cephalexin (clindamycin if MRSA is suspected); a fluctuant abscess is aspirated or drained.

Periductal mastitis. Seen in nonlactating women, and some men, who smoke. Squamous metaplasia of the lactiferous ducts produces keratin plugs, duct dilation and rupture; keratin spilled into the stroma provokes intense, sometimes granulomatous inflammation. Patients have a painful red subareolar mass or abscess, nipple inversion and fistula tracts to the areolar edge (Zuska disease when recurrent). Because drainage alone often fails, the involved duct is excised and smoking stopped.

Mammary duct ectasia. Older, usually multiparous women develop dilated subareolar ducts filled with inspissated secretions, surrounded by plasma-cell–rich chronic inflammation and fibrosis. Thick green, brown or white discharge from several ducts, periareolar induration, nipple retraction and rod-like calcifications can mimic carcinoma.

Fat necrosis. Blunt trauma such as a seatbelt injury, surgery or radiation damages breast fat, though many patients recall no injury. The result is a painless, firm, irregular mass with skin retraction and calcifications, including calcified oil cysts. Histology shows anucleate fat cells, foamy lipid-laden macrophages and giant cells; fatty acids released from dead adipocytes bind calcium (saponification), leaving chalky dystrophic calcification.

Male breast cancer

Risk factors. Men account for about 1% of breast cancers, usually in their 60s and 70s. BRCA2 is the strongest inherited risk (BRCA1 less so) and also brings pancreatic and prostate cancer risk. Klinefelter syndrome and other states of estrogen excess (cirrhosis, obesity, exogenous estrogen), chest radiation and family history also contribute.

Presentation and pathology. A hard, painless, unilateral subareolar mass, often eccentric and fixed, with nipple retraction, bloody discharge, or early skin and axillary node spread. Most tumors are invasive ductal carcinoma of no special type, more than 90% are ER-positive, and lobular carcinoma is rare because the male breast has few lobules. Tamoxifen is the standard endocrine therapy; an aromatase inhibitor alone suppresses estrogen incompletely in men and is paired with GnRH suppression if used.

Gynecomastia is not premalignant: it is bilateral, rubbery, tender and concentric beneath the nipple, whereas cancer is usually unilateral, hard and fixed.