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Expression of Sialyl‐Tn in fine‐needle aspirates from mammographically detected breast lesions: A marker of malignancy?
Author(s) -
Schmitt Fernando Carlos,
Marinho Antonio,
Amendoeira Isabel
Publication year - 1998
Publication title -
diagnostic cytopathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.417
H-Index - 65
eISSN - 1097-0339
pISSN - 8755-1039
DOI - 10.1002/(sici)1097-0339(199805)18:5<325::aid-dc3>3.0.co;2-9
Subject(s) - medicine , fibroadenoma , malignancy , pathology , apocrine , malignant transformation , fine needle aspiration , mucin , ductal carcinoma , biopsy , breast cancer , cancer
Malignant transformation is frequently associated with abnormal expression of cell surface carbohydrates. Sialyl‐Tn (STn) is a core carbohydrate antigen of tumor‐associated mucin formed by the premature 2‐6 sialylation of N‐acetylgalactosamine. In an attempt to verify whether this antigen is restricted to malignant cells, we studied 30 cases of fine‐needle aspiration (FNA) cytology from mammographically detected breast lesions. The rationale for choosing this material was the acknowledged difficulty in diagnosing cytologically small breast lesions, especially epithelial intraductal proliferations. The cases were divided in benign lesions (two fibroadenomas and ten ductal hyperplasias) and malignant lesions (16 ductal carcinomas). Ten of sixteen malignant cases (62.5%) were positive for STn. Five of fourteen benign cases (35.7%) were also positive for STn (two fibroadenomas and three ductal hyperplasias). The most consistent positive results in benign lesions resulted from cases that displayed apocrine metaplasia, although positivity has also been observed in ductal cells without metaplasia. We did not find statistical significant differences among STn expression in benign and malignant breast lesions detected by FNA ( P = 0.14). Thus, we conclude that STn is neither specific nor sensitive for detection of malignancy in FNA from mammographically detected breast lesions. Diagn. Cytopathol. 1998;18:325–329. © 1998 Wiley‐Liss, Inc.