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Smad3 and phospho-Smad3 are potential markers of invasive nonfunctioning pituitary adenomas

Authors Liu C, Li Z, Wu D, Li C, Zhang Y

Received 2 November 2015

Accepted for publication 8 February 2016

Published 15 April 2016 Volume 2016:9 Pages 2265—2271


Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Wei An

Peer reviewer comments 2

Editor who approved publication: Professor Min Li

Chunhui Liu,1,2 Zhenye Li,1–3 Dan Wu,4 Chuzhong Li,1–3 Yazhuo Zhang1–3

1Beijing Neurosurgical Institute, Capital Medical University, 2Beijing Institute for Brain Disorders, Brain Tumor Center, 3Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, 4Department of Neurology, Beijing Renhe Hospital, Beijing, People’s Republic of China

Background: Transforming growth factor-β (TGF-β) signaling plays important roles in tumor development. Nevertheless, the roles of TGF-β/Smad signaling in nonfunctioning pituitary adenomas (NFPAs) have not been fully studied.
Tumor samples were obtained from patients who had NFPAs and underwent endoscopic transsphenoidal surgery or craniotomy at Beijing Tiantan Hospital from March 2008 to December 2012. Immunohistochemistry was performed to determine the expression of Smad transducer proteins in NFPAs. Ki-67 was evaluated as an indicator of the proliferative activity of NFPAs.
Results: A total of 161 patients with NFPAs were identified; 59 (36.6%) had invasive NFPAs and 102 (63.4%) had noninvasive NFPAs. Protein levels of Smad3 and phospho-Smad3 (p-Smad3) were significantly lower in patients with invasive NFPAs than in patients with noninvasive NFPAs (P<0.05 and P<0.01, respectively). The Ki-67 index was markedly greater in invasive NFPAs than in noninvasive NFPAs (P<0.05) and was significant correlated with p-Smad3 levels (P<0.05, r=-0.702).
Conclusion: A low level of Smad3 and p-Smad3 proteins was associated with the invasion of NFPAs.

Keywords: nonfunctioning pituitary adenoma, invasion, transforming growth factor-β, Smad, Ki-67

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