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Polymerase chain reaction‐based detection of clonality as a non‐morphologic diagnostic tool for fine‐needle aspiration of the breast
Author(s) -
Magda Jessica L.,
Minger Brett A.,
Rimm David L.
Publication year - 1998
Publication title -
cancer cytopathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.052
H-Index - 304
eISSN - 1097-0142
pISSN - 0008-543X
DOI - 10.1002/(sici)1097-0142(19980825)84:4<262::aid-cncr12>3.0.co;2-q
Subject(s) - polymerase chain reaction , pathology , fine needle aspiration , medicine , monoclonal , breast cancer , biopsy , cancer , biology , monoclonal antibody , gene , antibody , genetics , immunology
BACKGROUND Fine‐needle aspiration (FNA) of breast specimens can be difficult and between 10‐25% of the lesions ultimately are classified as "atypical," even by the most experienced cytopathologist. The goal of this study was to identify a molecular mechanism that reliably distinguishes benign and malignant (or premalignant) lesions and that could be used as an adjunct in these morphologically ambiguous cases. METHODS Because all malignancies represent clonal proliferations, assessment of clonality represents a potential molecular mechanism for making this distinction. Excess material preserved from breast FNAs was examined using the human androgen receptor locus clonality assay. This assay allows determination of clonality on the basis of X chromosome inactivation as detected by polymerase chain reaction analysis of genomic DNA after methylase‐sensitive restriction digestion. RESULTS In this pilot study, 25 cases showed reproducible results. All malignant cases (9 of 9) were monoclonal, whereas 10 of 12 benign cases were polyclonal. Of four atypical cases, two were monoclonal and both were found to be malignant after surgical resection. Monoclonality was observed in two benign cases that were hyperplastic lesions. CONCLUSIONS These preliminary results suggest that this test may provide a non‐morphologic molecular mechanism for the objective categorization of breast FNAs. Cancer (Cancer Cytopathol) 1998;84:262‐267. © 1998 American Cancer Society.