The age of onset of cystic hyperplasia of the breast generally begins at 30 to 34 years of age; 40 to 49 years of age is the peak of the onset of young women is rare, and the incidence decreases rapidly after menopause. Its incidence is 5% to 9% in adult women. Coormaghtigi and Amerlinck demonstrated in 1930 that ovariectomized rats injected with estrogen could produce cystic mammary gland disease. In humans, estrogen not only stimulates mammary epithelial hyperplasia but also causes dilation of the ducts and the formation of cysts. Recent studies suggest that hyperprolactinemia is an important cause of cystic hyperplasia of the breast, and foreign scholars have reported that cystic hyperplasia of the breast in postmenopausal women is often the result of inappropriate estrogen replacement therapy. Pathogenesis: The pathological changes in cystic hyperplasia of the breast are characterized by: 1. Gross morphology: cystic nodules or masses of varying size and hardness in the breast tissue on one or both sides. Cysts vary in size, with large cysts up to 1-125 px in diameter being grayish or blue, also known as blue domed cysts or blue-topped cysts (Figure 1) Small cysts are mostly seen around large cysts, only 2 mm in diameter, not even visible to the naked eye, and only visible under the microscope. Incision of large cysts reveals cyst contents as clear, colorless, plasma or brownish-yellow fluid, sometimes bloody. It contains proteins, hormones (lactogen, estrogen, androgens, human chorionic gonadotropin, human growth hormone, follicle stimulating hormone, luteinizing hormone, etc.), sugars, minerals and cholesterol. The cystic wall is thick and lusterless, with granular or papillary tumor-like material protruding into the cystic cavity. 2. Histological pattern: 5 different lesions can be seen: (1) Cyst: terminal duct and alveolar hyperplasia, small duct expansion and extension, terminal duct cyst formation. The terminal duct epithelium abnormally proliferates to form multiple layers from the duct wall to the lumen for papillary growth, occupying most of the duct lumen, so that the lumen is obstructed and dilated by secretion retention, and cysts are formed (Figure 2). Cysts can be divided into simple cysts with only cystic expansion without epithelial hyperplasia; and another kind of papillary cysts with papillary epithelial hyperplasia. (2) Epithelial hyperplasia of milk ducts: the epithelium in dilated ducts and cysts shows different degrees of hyperplasia, with the lighter ones showing increased epithelial layers and the heavier ones showing papillary protrusions, or connected to each other in a reticular or sieve-like, solid, or glandular pattern. If the cyst epithelium is actively proliferating, atypical hyperplasia or interstitial changes are common and may develop into cancer. (3) Papillomatosis: that is, on the basis of the cystic expansion of papillary cysts, the epithelial cells of the cyst wall are papillary proliferated in many places to form papillomatosis According to the papillary density and the degree of epithelial cell proliferation in the affected area of papillomatosis, papillomatosis can be classified as mild to moderate and severe, which has practical significance in clinical practice. (4) Glandular duct-type adenopathy: lobular ducts or alveolar ducts are chemotactic and hyperplastic, with solid masses of proliferating epithelial cells and varying degrees of proliferation of fibrous tissue, while ductal dilatation and cyst formation are not evident, called adenopathy formation. (5) Sweat gland-like metaplasia: the cyst wall is covered with epithelial metaplasia in a high columnar shape, rich in cytoplasm, which has eosinophilic granules, resembling sweat gland cells, the appearance of such cells is often a benign sign. In addition, the cyst wall, ducts, and fibrous tissue around the vesicles proliferate and form fibrous cords that squeeze the surrounding ducts to produce obstruction, leading to retention of secretions and then cause distortion or expansion of the ducts (Figure 3). 3. Pathological diagnostic criteria: cystic hyperplasia of the breast has the above five lesions, which do not exist simultaneously, of which papillomatosis ductal adenopathy and cysts are the main lesions. The rate of occurrence of various lesions is related to the site of tissue sampling and the amount of sampling. If three of the five lesions or two of the three major lesions can be seen in the section, the diagnosis is made. Among the 5 lesions cystic ductal epithelial hyperplasia, papillomatosis, and atypical hyperplasia due to adenoidal adenopathy are prone to carcinogenesis.