1. ¹Division of Pathology and Laboratory Medicine, European Institute of Oncology and University of Milan, School of Medicine, Milan, Italy
2. ²Department of Pathological Anatomy and Genetics, University of Bari, School of Medicine, Bari, Italy
3. ³Division of Pathology, Regional Hospital, Treviso, Italy
4. ⁴Division of Senology, European Institute of Oncology, Milan, Italy

Correspondence: Professor G Viale, MD, FRCPath, Division of Pathology and Laboratory Medicine, European Institute of Oncology, Via Ripamonti, 435, 20141 Milan, Italy. E-mail: giuseppe.viale@ieo.it

Received 1 December 2004; Revised 17 December 2004; Accepted 20 December 2004; Published online 22 April 2005.

Abstract

Adenoid cystic carcinoma of the breast represents a unique clinicopathologic entity with a variable histological appearance and a relatively indolent clinical course in most of the cases. Adenoid cystic carcinoma may be difficult to differentiate from infiltrating duct carcinomas, and in particular from tubular and cribriform carcinomas, especially in core or vacuum-assisted biopsies. We evaluated the prevalence of c-kit, p63, and e-cadherin immunoreactivity in a series of 20 adenoid cystic carcinomas, comparing the results with those obtained in a series of infiltrating tubular carcinomas and infiltrating cribriform carcinomas. The hormone receptor status, proliferation labeling index, and HER/2 immunoreactivity had been previously investigated in all the cases. Three (15%) adenoid cystic carcinomas and all infiltrating tubular and cribriform carcinomas showed estrogen receptor and/or progesterone receptor immunoreactivity (P<0.00001 for estrogen and P=0.00002 for progesterone receptors). Adenoid cystic carcinomas consistently lacked any immunoreactivity for HER/2, whereas three (15%) infiltrating and cribriform carcinomas showed weak and incomplete membrane staining (P=0.23077). Membranous immunoreactivity for c-kit was found in all except one (predominantly basaloid) adenoid cystic carcinomas (95%), and in none of the infiltrating tubular and cribriform carcinomas (P<0.00001). Nuclear immunoreactivity for p63 was found in all except three (predominantly basaloid) adenoid cystic carcinomas (85%) and in none of the infiltrating tubular and cribriform carcinomas (P<0.00001). All infiltrating tubular and cribriform carcinomas and 18/20 (90%) adenoid cystic carcinomas showed immunoreactivity for e-cadherin (P=0.48718). In summary, adenoid cystic carcinomas showed the following phenotype: estrogen receptor^-/progesterone receptor^-/c-kit⁺/p63⁺ (13 cases, 65%), estrogen receptor^-/progesterone receptor/c-kit⁺/p63^- (three cases, 15%), estrogen receptor^-/progesterone receptor^-/c-kit^-/p63⁺ (one case, 5%), estrogen receptor⁺/progesterone receptor⁺/c-kit⁺/p63⁺ (two cases, 10%), and estrogen receptor⁺/progesterone receptor^-/c-kit⁺/p63⁺ (one case). By contrast, all the infiltrating tubular and cribriform carcinomas showed the estrogen receptor⁺/progesterone receptor⁺/c-kit^-/p63^- phenotype. Our data provide evidence that immunoreactivity for c-kit and/or p63 may be useful in differentiating adenoid cystic carcinomas from other types of breast cancer.