Immunohistochemistry of cyclin D1 and beta-catenin, and mutational analysis of exon 3 of beta-catenin gene in parathyroid adenomas.
Parathyroid adenomas are benign uniglandular tumors and are the most common cause of primary hyperparathyroidism. Several genetic changes in parathyroid tumors, including inactivation of tumor suppressor genes, activation of oncogenes and loss of heterozygosity at several chromosomal loci, have been reported. In this study, we analyzed the status of cyclin D1 and beta-catenin in 24 cases of parathyroid adenoma. Immunohistochemistry of cyclin D1 showed positive staining in 9 (37.5%) of the 24 parathyroid adenomas. The status of beta-catenin, which has recently been identified as a regulator of cyclin D1 transcription, was examined by direct sequencing of exon 3 of the beta-catenin gene and immunohistochemistry of beta-catenin protein, but neither mutation nor accumulation of beta-catenin was detected in any of the cases. These results indicate that cyclin D1 is frequently accumulated in parathyroid adenomas, independently of dysfunction in the Wnt signaling pathway.
Ikeda
Satoshi
S
Second Department of Surgery, Hiroshima University Faculty of Medicine, Hiroshima 734-8551, Japan. sikeda@hiroshima-u.ac.jp
Ishizaki
Yasuyo
Y
Shimizu
Yosuke
Y
Fujimori
Masahiko
M
Ojima
Yasutomo
Y
Okajima
Masazumi
M
Sugino
Keizo
K
Asahara
Toshimasa
T
D000236:Adenoma / Q000235:genetics* / Q000378:metabolism*; D002448:Cell Adhesion; D019938:Cyclin D1 / Q000096:biosynthesis* / Q000235:genetics*; D003598:Cytoskeletal Proteins / Q000096:biosynthesis* / Q000235:genetics*; D004252:DNA Mutational Analysis; D005091:Exons; D006801:Humans; D007150:Immunohistochemistry; D009154:Mutation; D010282:Parathyroid Neoplasms / Q000235:genetics* / Q000378:metabolism*; D015398:Signal Transduction; D015534:Trans-Activators; D014158:Transcription, Genetic; D051176:beta Catenin
C495270:CTNNB1 protein, human; D003598:Cytoskeletal Proteins; D015534:Trans-Activators; D051176:beta Catenin; D019938:Cyclin D1