A role for the pituitary tumor-transforming gene in the genesis and progression of non-small cell lung carcinomas

• Published in: Anticancer research Vol. 23; no. 5A; p. 3775
• Main Authors: Honda, Shoko, Hayashi, Moriaki, Kobayashi, Yasuhito, Ishikawa, Yuichi, Nakagawa, Ken, Tsuchiya, Eiju
• Format: Journal Article
• Language: English
• Published: Greece 01.09.2003
• Subjects: Adult; Aged; Aged, 80 and over; Carcinoma, Non-Small-Cell Lung - genetics; Carcinoma, Non-Small-Cell Lung - metabolism; Carcinoma, Non-Small-Cell Lung - pathology; Chromosome Aberrations; Disease Progression; Female; Fibroblast Growth Factor 2 - biosynthesis; Humans; Immunohistochemistry; Lung Neoplasms - genetics; Lung Neoplasms - metabolism; Lung Neoplasms - pathology; Male; Middle Aged; Neoplasm Proteins - biosynthesis; Neoplasm Proteins - genetics; Nucleic Acid Hybridization; RNA, Messenger - biosynthesis; RNA, Messenger - genetics; Securin
• ISSN: 0250-7005

The product of the pituitary tumor-transforming gene (PTTG) inhibits chromatid separation, which is considered to promote chromosome instability, especially in the absence of the p53 gene product, and also induces basic fibroblast growth factor (bFGF) production. Its expression and these variables in primary non-small cell carcinomas (NSCLCs) of known p53 status were examined. Comparative genomic hybridization analysis of 78 lesions revealed a wide range of total (gain + loss) chromosomal imbalance numbers (tCINs). Seven each with the highest and lowest tCINs were examined for PTTG mRNA by semi-quantitative RT-PCR and bFGF production immunohistochemically. Mean relative values for PTTG mRNA for the tumors and corresponding normal lung tissues were 1.46 and 0.88, respectively, the difference being statistically significant. Overexpression of bFGF was observed in 12 out of 14 with intense immunostaining of carcinoma cells, in contrast to the weak or lack of staining in normal lung tissues. However, relative PTTG values did not correlate with tCINs or immunoreactivity for bFGF among the tumors regardless of the p53 status. The results indicate that overexpression of PTTG plays a role in the genesis and progression of NSCLCs, although its effects on CINs and bFGF production may be obscured by other complicating factors.