title: Is lobular endocervical glandular hyperplasia a cancerous precursor of minimal deviation adenocarcinoma?: a comparative molecular-genetic and immunohistochemical study.
abstract: Although lobular endocervical glandular hyperplasia (LEGH) was originally described as a distinct hyperplastic glandular lesion of the uterine cervix, recent studies have raised a question that LEGH may be a cancerous precursor of minimal deviation adenocarcinoma (MDA) and other mucinous adenocarcinomas (MACs) of the uterine cervix. In the present study, we studied LEGH, MDA, and MAC by using molecular-genetic and immunohistochemical methods for chromosomal imbalance, microsatellite instability, human papillomavirus (HPV) infection, and gastric pyloric-type mucin secretion to clarify their relationship. Comparative genomic hybridization revealed recurrent chromosomal imbalances, that is, gains of chromosome 3q and a loss of 1p, which were common to MDA and MAC, in 3 of 14 LEGHs analyzed (21%). LEGHs with chromosomal imbalances showed a degree of cellular atypia in the hyperplastic glandular epithelium. Dual-color fluorescence in situ hybridization confirmed a gain of chromosome 3 fragment in these cervical glandular lesions. HPV in situ hybridization revealed that high-risk HPV (types 16 and 18) was positive in over 80% of MACs, but negative in all LEGHs and MDAs examined. Microsatellite instability was rarely detected in these cervical glandular lesions. Our present study results demonstrated a molecular-genetic link between LEGH and cervical mucinous glandular malignancies including MDA and MAC, and are thought to support the hypothesis that a proportion of LEGHs are cancerous precursors of MDA and/or MAC.
authors.affiliation: Department of Pathology, Yamaguchi University Graduate School of Medicine, Yamaguchi, Japan. shig@yamaguchi-u.ac.jp
authors.forename: Shigeto
authors.initials: S
authors.lastname: Kawauchi
authors.forename: Tomoko
authors.initials: T
authors.lastname: Kusuda
authors.forename: Xu-Ping
authors.initials: XP
authors.lastname: Liu
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Suehiro
authors.forename: Tsunehisa
authors.initials: T
authors.lastname: Kaku
authors.forename: Yoshiki
authors.initials: Y
authors.lastname: Mikami
authors.forename: Morishige
authors.initials: M
authors.lastname: Takeshita
authors.forename: Motonao
authors.initials: M
authors.lastname: Nakao
authors.forename: Yasuyo
authors.initials: Y
authors.lastname: Chochi
authors.forename: Kohsuke
authors.initials: K
authors.lastname: Sasaki
mesh_terms: D000230:Adenocarcinoma / Q000235:genetics / Q000473:pathology* / Q000821:virology; D000328:Adult; D000368:Aged; D002584:Cervix Uteri / Q000473:pathology*; D055028:Comparative Genomic Hybridization; D005260:Female; D006801:Humans; D006965:Hyperplasia; D007150:Immunohistochemistry; D017404:In Situ Hybridization, Fluorescence; D053842:Microsatellite Instability; D008875:Middle Aged; D030361:Papillomavirus Infections; D016133:Polymerase Chain Reaction; D011230:Precancerous Conditions / Q000235:genetics / Q000473:pathology* / Q000821:virology; D002583:Uterine Cervical Neoplasms / Q000235:genetics / Q000473:pathology* / Q000821:virology