2022
DOI: 10.1016/j.inat.2021.101374
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Expression of IL-6 and matrix metalloproteinases in a convexity meningiomas with hyperostosis: Case report

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Cited by 2 publications
(10 citation statements)
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“…IL-6 is produced by meningioma cells but does not stimulate tumor growth, whereas IL-6 mediates the differentiation of osteoblast and osteocytes into osteoclasts. Therefore, the role of IL-6 in hyperostosis in meningiomas is attributed to the effect of bone resorption rather than to tumor cell growth [32], [37]. The limitation of our study is that it did not examine IL-6 expression associated with the mechanism of hyperostosis.…”
Section: Discussionmentioning
confidence: 93%
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“…IL-6 is produced by meningioma cells but does not stimulate tumor growth, whereas IL-6 mediates the differentiation of osteoblast and osteocytes into osteoclasts. Therefore, the role of IL-6 in hyperostosis in meningiomas is attributed to the effect of bone resorption rather than to tumor cell growth [32], [37]. The limitation of our study is that it did not examine IL-6 expression associated with the mechanism of hyperostosis.…”
Section: Discussionmentioning
confidence: 93%
“…MMP is a calcium-dependent zinc-containing endopeptidase that degrades extracellular matrix (ECM) and is involved in the penetration of tumor cells into adjacent tissues. This molecule initiates angiogenesis and the bioactive processes of proteins such as cytokines, chemokines, and cell surface receptors [32]. Bone is mainly composed of type I, type V, and type VI collagen.…”
Section: Discussionmentioning
confidence: 99%
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“…In human patients with CH, meningiomas have been shown to express high levels of IL-6, MMP-1, MMP-2, and MMP-9 with minimal expression of these molecular factors in normal brain parenchyma. 18,19 The pro-inflammatory effects of tumour-expressed IL-6 include activation JAK/STAT, PI3K/AKT, and MAPK pathways, and through these pathways osteoclast activation occurs resulting in bone destruction and resorption, which may allow tumour extension into the calvarium. 19,27 The role of tumour derived IL-6 contributing to CH in humans is further supported from the observation that tumours do not regrow, and CH does not progress, when calvarial bone is replaced following tumour resection.…”
Section: Meningiomas With Microscopic Evidence Of Calvarial Invasionmentioning
confidence: 99%
“…16,17 Elaboration of matrix metalloproteinases (MMP) 2-and À9, interleukin-6 (IL-6), and alkaline phosphatase (ALP) by the tumour have all been implicated as potential molecular mediators of CH in human meningiomas. [17][18][19] The objectives of this study were to describe the prevalence and imaging characteristics of CH in a population of cats with intracranial meningiomas, investigate possible associations of tumour histopathologic and molecular characteristics with the presence of CH, and compare progression free survival times (PFS) between cats with and without CH that were treated surgically. It was hypothesised that: (1) CH would be associated with histologic evidence of tumour invasion into the skull; (2) tumour expression of MMP-2, MMP-9, and IL-6 would be higher in cats with CH; (3) serum bonespecific alkaline phosphatase (ALP) concentrations would be higher in cats with CH; and (4) progression free survival time (PFS) following surgical treatment of meningioma would be superior in cats without CH.…”
Section: Introductionmentioning
confidence: 99%