Document Detail

PTTG overexpression is correlated with angiogenesis in human pituitary adenomas.
MedLine Citation:
PMID:  17159247     Owner:  NLM     Status:  MEDLINE    
Human pituitary tumor transforming gene (hPTTG1) was recently identified as a protooncogene, which is a regulator of the cell cycle, as a homolog of yeast securin and a transcriptional activator of several angiogenic factors. Here we examined the relationships of hPTTG1 expression with cell proliferation, expression of the angiogenic factor, VEGF (vascular endothelial growth factor), and numbers of the blood vessels in the normal and/or adenomatous pituitary. With the exception of TSHoma, the expression of hPTTG1 was significantly higher in pituitary adenomas than in the normal pituitary gland. The cell proliferation activity was higher in pituitary adenomas than in the normal pituitary. Pituitary cell proliferation was significantly correlated with the level of hPTTG1 expression in the normal pituitary tissue, but there was no such correlation in the adenomas. The significant correlation of hPTTG1 with the VEGF expression and the numbers of the blood vessels was elucidated in pituitary adenomas. It is particularly noteworthy that immunohistochemical double staining indicated co-localization of VEGF in many hPTTG1-positive tumor cells. In conclusion, higher levels of hPTTG1 expression contribute to the pathobiology of pituitary adenomas by promoting angiogenesis rather than by activating cell proliferation, whereas hPTTG1 expression is related to mitotic activity in the normal pituitary gland.
Takeo Minematsu; Masanori Suzuki; Naoko Sanno; Susumu Takekoshi; Akira Teramoto; R Yoshiyuki Osamura
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Endocrine pathology     Volume:  17     ISSN:  1046-3976     ISO Abbreviation:  Endocr. Pathol.     Publication Date:  2006  
Date Detail:
Created Date:  2006-12-12     Completed Date:  2007-02-01     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9009288     Medline TA:  Endocr Pathol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  143-53     Citation Subset:  IM    
Department of Pathology, Tokai University School of Medicine. Bohseidai, Isehara, Kanagawa 259-1193, Japan.
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MeSH Terms
Adenoma / blood supply,  metabolism*,  pathology
Apoptosis / physiology
Cell Proliferation
Neoplasm Proteins / biosynthesis*
Neovascularization, Pathologic / metabolism*
Pituitary Neoplasms / blood supply,  metabolism*,  pathology
RNA, Messenger / analysis
Reverse Transcriptase Polymerase Chain Reaction
Vascular Endothelial Growth Factor A / metabolism
Reg. No./Substance:
0/Neoplasm Proteins; 0/RNA, Messenger; 0/Vascular Endothelial Growth Factor A; 0/pituitary tumor-transforming proteins

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