Papillary mucinous metaplasia: a distinct precursor of mucinous adenocarcinoma of the endometrium

xlomafota13 shared this article with you from Inoreader Papillary mucinous metaplasia: a distinct precursor of mucinous adenocarcinoma of the endometrium Via International Journal of Clinical and Experimental Pathology Int J Clin Exp Pathol. 2022 Feb 15;15(2):83-87. eCollection 2022. ABSTRACT Mucinous adenocarcinoma of the endometrium is heterogeneous, consisting of endometrioid adenocarcinoma composed of >50% mucinous cells, low-grade mucinous adenocarcinoma, microglandular adenocarcinoma, and gastric (gastrointestinal)-type adenocarcinoma. Previous studies have reported that papillary mucinous metaplasia is a possible precancerous lesion of mucinous adenocarcinoma with frequent KRAS mutations. Recently, we encountered a case of pure mucinous adenocarcinoma of the endometrium with concurrent papillary mucinous metaplasia in a 35-year-old woman. She underwent 6-month hormonal therapy for atypical endometrial hyperplasia. A follow-up biopsy led to a diagnosis of mucinous adenocarcinoma; therefore, total hysterectomy was performed. The tumor showed abundant intracytoplasmic mucin and mild-to-moderate cytologic atypia with papillary architectu re. KRAS mutation analysis revealed a point mutation from GGT to GTT in codon 12. Although papillary mucinous metaplasia showed an overexpression of p16INK4, especially in the intragrandular papillary tufts, and a low MKi67 labeling index, overt mucinous adenocarcinoma with a loss of P16INK4a expression showed a high proliferating index of MKI67. The mass presented with stage ІA disease. During follow-up, the patient was stable and showed no recurrence. Considering the histologic similarity and incidence of KRAS mutations between papillary mucinous metaplasia and mucinous adenocarcinoma, papillary mucinous metaplasia may be a precancerous lesion for a subset of mucinous adenocarcinoma of the endometrium. PMID:35265257 | PMC:PMC8902477 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.