Clonality assessment of adenomatoid tumor supports its neoplastic nature

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• 作者：Wei Wang ; MS^a ; ¹ ; Huiting Zhu ; PhD^b ; ¹ ; Jigang Wang ; PhD^a ; Shuyang Wang ; PhD^a ; Diyi Wang ; MS^c ; Jingjing Zhao ; MS^b ; Hongguang Zhu ; PhD^a ; ^d ; ^{hongguang_701@shmu.edu.cn" class="auth_mail" title="E-mail the corresponding author}
• 关键词：Adenomatoid tumor ; Clonality ; Human androgen receptor gene ; Laser capture microdissection ; Mesothelial hyperplasia ; X-chromosome inactivation
• 刊名：Human Pathology
• 出版年：2016
• 出版时间：February 2016
• 年：2016
• 卷：48
• 期：Complete
• 页码：88-94
• 全文大小：1059 K

文摘

Adenomatoid tumor is a relatively rare disease that predominantly involves male and female internal genital tracts. Although its clinical and pathologic features are well characterized, there is still controversy regarding its nature as a true neoplasm or a variant of mesothelial hyperplasia of a reactive nature. We sought to resolve this debate by investigating the clonality of uterine adenomatoid tumor from 13 female cases. The mesothelial cells and surrounding normal myometrium were precisely harvested using laser capture microdissection, and genomic DNA was extracted for clonal analysis by assessing the patterns of X-chromosome inactivation. Fluorescent polymerase chain reaction amplification of a highly polymorphic short tandem repeat of the human androgen receptor (HUMARA) gene with and without methylation-sensitive restriction endonuclease HpaII digestion was performed on DNA extracted from mesothelial cells, using normal myometrium and male blood sample as controls. Of the 13 cases successfully amplified, all 10 informative cases showed concordant nonrandom X-chromosome inactivation pattern consistent with monoclonality. In comparison, surrounding normal myometrium showed a polyclonal pattern of X-chromosome inactivation, and male blood sample failed to be amplified after HpaII treatment. Our results demonstrate that adenomatoid tumor is a monoclonal disease favoring a neoplastic process. This neoplastic rather than reactive nature probably accounts for its frequently observed infiltrative growth pattern and the occurrence of diffuse adenomatoid tumor, especially when host immunity is compromised. Additional studies with larger sample sizes will be needed to conclusively prove our conclusion.