title: Morphological characterization and subtyping of silent somatotroph adenomas.
abstract: GH-producing adenomas clinically are endocrine-active tumors accompanied with acromegaly in most instances. However, GH-producing adenomas apparently unassociated with acromegaly, or so-called silent somatotroph adenomas (SSA), have recently been reported but rarely. The reported cases are characterized by normal or slightly elevated serum levels of GH but without acromegaly. Tumor cells contain moderate, trace or no GH immunoreactivity. We experienced 7 cases of SSA which were not always similar in morphology and pathogenetic mechanism. They could be further divided into the following 3 subtypes. Subtype 1 (N = 2): a moderate number of cells were immunopositive for GH, and GH mRNA was also expressed in moderate or numerous cells. Densely granulated cells were noted. It is assumed that inhibition of hormone release into circulation. Subtype 2 (N = 3): a small number of cells were immunopositive for GH, while GH mRNA was expressed in numerous tumor cells. They were sparsely granulated cells containing fibrous bodies. These findings suggest that posttranslational processing of the gene product may be defective. Subtype 3 (N = 2): Only a scattered number of cells were immunopositive for GH and GH mRNA was co-localized in immunopositive cells. They were sparsely granulated cells containing poorly developed organelles that did not resemble those of typical sparsely granulated GH cells. The findings indicate that adenoma cells are largely immature with minimal GH lineage differentiation.
authors.affiliation: Department of Pathology, Kitasato University School of Medicine, Kanagawa, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Naritaka
authors.forename: T
authors.initials: T
authors.lastname: Kameya
authors.forename: Y
authors.initials: Y
authors.lastname: Sato
authors.forename: S
authors.initials: S
authors.lastname: Furuhata
authors.forename: M
authors.initials: M
authors.lastname: Otani
authors.forename: T
authors.initials: T
authors.lastname: Kawase
mesh_terms: D000172:Acromegaly / Q000209:etiology; D000236:Adenoma / Q000235:genetics / Q000473:pathology* / Q000503:physiopathology*; D000328:Adult; D000368:Aged; D002648:Child; D005260:Female; D019382:Human Growth Hormone / Q000096:biosynthesis* / Q000235:genetics / Q000378:metabolism; D006801:Humans; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D019394:Ki-67 Antigen / Q000378:metabolism; D008297:Male; D016253:Microscopy, Immunoelectron; D008875:Middle Aged; D010908:Pituitary Hormones, Anterior / Q000378:metabolism; D010911:Pituitary Neoplasms / Q000235:genetics / Q000473:pathology* / Q000503:physiopathology*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D012334:RNA, Neoplasm / Q000235:genetics / Q000378:metabolism; D013973:Thyrotropin-Releasing Hormone; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism
chemical_list: D019394:Ki-67 Antigen; D010908:Pituitary Hormones, Anterior; D012333:RNA, Messenger; D012334:RNA, Neoplasm; D016159:Tumor Suppressor Protein p53; D019382:Human Growth Hormone; D013973:Thyrotropin-Releasing Hormone