Expression of cell cycle regulators and biomarkers of proliferation and regrowth in human pituitary adenomas View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2017-03-24

AUTHORS

Mark Gruppetta, Robert Formosa, Sharon Falzon, Sabrina Ariff Scicluna, Edward Falzon, James Degeatano, Josanne Vassallo

ABSTRACT

PurposeThe pathogenesis of pituitary adenomas (PA) is complex. Ki-67, pituitary tumour transforming gene (PTTG), vascular endothelial growth factor (VEGF), cyclin D1, c-MYC and pituitary adenylate cyclase-activating peptide (PACAP) protein expression were analysed and correlated with tumour and patient characteristics.Methods74 pituitary tumour samples (48 non-functional PA, 26 functional PAs); Immunohistochemical analysis of protein expression, retrospective analysis of MR images and in vitro analysis of octreotide treatment was carried out on GH3 cells.ResultsPTTG expression was negatively associated with age and positively with PA size, regrowth and Ki-67 index. Cyclin D1 correlated with Ki-67 and tumour size. c-MYC negatively correlated with size of tumour and age; and correlated with PTTG expression. Somatostatin analogue treatment was associated with lower Ki-67, PTTG and Cyclin D1 expression while T2 hypointense PAs were associated with lower PTTG, cyclin D1, c-MYC and Ki-67. In vitro analyses confirmed the effect of somatostatin analogue treatment on Pttg and Cyclin D1 expression.ConclusionsInteresting and novel observations on the differences in expression of tumour markers studied are reported. Correlation between Ki-67 expression, PTTG nuclear expression and recurrence/regrowth of PAs, emphasizes the role that Ki-67 and PTTG expression have as markers of increased proliferation. c-MYC and PTTG nuclear expression levels were correlated providing evidence that PTTG induces c-MYC expression in PAs and we propose that c-MYC might principally have a role in early pituitary tumorigenesis. Evidence is shown that the anti-proliferative effect of somatostatin analogue treatment in vivo occurs through regulation of the cell cycle. More... »

PAGES

358-371

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s11102-017-0803-0

DOI

http://dx.doi.org/10.1007/s11102-017-0803-0

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1084029581

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/28342098


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