Abstract

Jayaram G
Department of Pathology, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia

A wide range of proliferative breast lesions can show papillary architecture. Broadly these may be categorized into neoplastic (benign and malignant) and non-neoplastic papillary proliferations. Non-neoplastic proliferations include florid papillomatosis of nipple, papillary apocrine metaplasia in fibrocystic condition (FCC) and micropapillary hyperplasia as a part of epithelial proliferative disease.

Duct papillomas (DP) are usually single and central, often cystic and may be brought to attention due to nipple discharge. They may be intraductal or subareolar and multiple associated lesions may be present in contiguous ducts. The branching fibrovascular stroma that supports the epithelial cells is overgrown in a few cases, leading to solid papillomas. Myoepithelium is always present, but may be attenuated in sclerosing lesions. Nipple discharge cytology often gives a clue to the diagnosis of a duct papilloma. Papillary adenoma of the nipple can simulate Paget’s disease and may show a papillomatous or adenosis pattern. Papillary apocrine metaplasia in FCC may show micropapillae or branching true papillae. Micropapillary hyperplasia is a part of the spectrum of epithelial proliferative disease encompassing moderate epithelial hyperplasia through atypical ductal hyperplasia (ADH) and intraductal carcinoma (DCIS). These lesions do not have fibrovascular cores.

Papillary carcinomas (PC) comprise 1-2% of breast carcinomas and are seen in an older age group than the usual (NOS) type of breast carcinoma. Nearly half involve the central part of the breast and so bleeding from nipple is more common than in DP. They are usually 2-3 cm in size but large cystic tumors may fill the breast. Partly clotted blood and detached papillary fragments are present in large cystic tumors and extensive sampling may be required to rule out invasion. Papillary fronds are a must to make a diagnosis of PC. Solid PCs arise by the overgrowth of cell proliferation that may largely outgrow the papillary pattern. The stroma in PC is less as compared to DP with loss of polarity of the epithelium, high nuclear cytoplasmic ratio and hyperchromatic nuclei. Mitoses are variable but usually more than 1 per 10 high power fields. Apocrine metaplasia is less frequent than in DP and is often atypical and myoepithelium is either absent or minimal. Grey-zone (borderline) lesions show areas of benign papillary proliferation along with more cellular and atypical areas and carry a four-fold increased risk of invasive carcinoma.

Mucin may be seen in small amounts in many PCs. When extracellular mucin is abundant, it may resemble mucinous carcinoma (MC). The invasive component in solid PC may be a MC in its entirety. Solid PCs may also show a pushing pattern of invasion without any reactive stromal changes. Invasion in PC is difficult to determine due to hemorrhage and fibrosis both within and at the boundary of the tumor. Artifacts due to fine needle aspiration or core biopsy such as hemorrhage, acute inflammation and unnatural fragmentation with tumor cells along the needle track may compound the difficulty. Extension of tumor into mammary parenchyma and fat are reliable evidences of invasion.