<p class="first" id="d19597806e166">The molecular mechanisms underlying the formation
of nonfunctioning pituitary adenomas
(NFAs) are largely unknown. In this study, we aimed to understand the relationship
between NFAs and functional pituitary adenomas and the possible role of proteins involved
in cell cycle, senescence, and DNA damage control mechanisms in the etiology of NFA.
We analyzed pATM-S1981, pRb-S608, Rb, pE2F1-S364, p16, E2F1, p73, cyclin D1, and CHEK2
protein expression (in a group of 20 patients with acromegaly, 18 patients with Cushing's
disease (CD), and 29 NFA patients) by immunohistochemistry and their relevant mRNA
expression by qRT-PCR (in a group of 7 patients with acromegaly, 7 patients with CD,
and 7 NFA patients). The clinical and histopathological results on the patients were
statistically evaluated. pE2F1-S364 protein expression in the CD group was significantly
lower than that in the NFA and acromegaly groups (p = 0.025, p = 0.034, respectively).
However, the expression of the p16 protein was lower than in the NFA group than in
the CD and acromegaly groups (p = 0.030, p = 0.033, respectively), and E2F1 protein
expression was significantly higher in the NFA group than in the CD group (p = 0.025).
p73 protein expression in patients with acromegaly was significantly higher (p = 0.031)
than that in the CD group. CHEK2 mRNA expression in the CD group was significantly
higher than that in the acromegaly group (p = 0.012). The selective and tumor-specific
associations between E2F1, pE2F1-S364, CHEK2, and p73 mRNA and protein levels indicate
their involvement in pituitary adenoma formation in NFA, CD, and acromegaly patients.
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