Elsevier

Human Pathology

Volume 31, Issue 4, April 2000, Pages 498-503
Human Pathology

Original contribution
Molecular evidence that the stromal andepithelial cells in pleomorphic adenomas of salivary gland arise from the same origin: clonal analysis using Human Androgen Receptor Gene (HUMARA) Assay*

https://doi.org/10.1053/hp.2000.6716Get rights and content

Abstract

Salivary gland pleomorphic adenomas are characterized by abiphasic growth of “epithelial” and “stromal” regions. The “epithelial” region is a compactly organized mixture of both luminal and nonluminal cells, whereas the stromal region is composed predominantly of the nonluminal cells. Using the polymerase chain reaction (PCR)-based HUMARA assay on DNA from formalin-fixed, paraffin embedded tissues from pleomorphic adnomas of female patients, we intend to clarify the clonal relation between the luminal and nonluminal cells and the clonal nature of the morphologically diverse nonluminal cells in this tumor. HUMARA, the human androgen receptor gene, is located on the X chromosome and contains a segment of polymorphic CAG tandem repeats in exon 1. Several methylationsensitive HhaI restriction sites are located 5' to these CAG repeats. It is an ideal tool to study clonality of female tissues by examining the methylation pattern. Of the 13 cases analyzed, 3 were homozygous at the HUMARA locus and therefore noninformative. The remaining 10 cases were informative. All 10 cases showed a monoclonal pattern in the stromal area, indicating that the morphologically diverse nonluminal cells are monoclonal. Eight of the 10 cases showed monoclonality in the “epithelial” areas, suggesting a common clonality between luminal and nonluminal cells. Of the remaining 2 samples, 1 was polyclonal for the “epithelial” region, and the other was not amplifiable. Our data provide the first molecular evidence that the luminal and nonluminal cells in pleomorphic adenomas arise from the same clone in most cases, and the morphologically diverse nonluminal cells are monoclonal.

Preliminary results of this work have been presented in theAnnual Meeting of the Association for Molecular Pathology, Crystal City, VA, November 1998.

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    *

    Supported by a grant from Harvey E. Nussbaum, MD, Research Institute of Saint Barnabas Medical Center.

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