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Molecular Network Basis of Invasive Pituitary Adenoma: A Review

机译:侵袭性垂体腺瘤的分子网络基础:综述。

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摘要

Cases with pituitary adenoma comprise 10–25% of intracranial neoplasm, being the third most common intracranial tumor, most of the adenomas are considered to be benign. About 35% of pituitary adenomas are invasive. This review summarized the known molecular basis of the invasiveness of pituitary adenomas. The study pointed out that hypoxia-inducible factor-1α, pituitary tumor transforming gene, vascular endothelial growth factor, fibroblast growth factor-2, and matrix metalloproteinases (MMPs, mainly MMP-2, and MMP-9) are core molecules responsible for the invasiveness of pituitary adenomas. The reason is that these molecules have the ability to directly or indirectly induce cell proliferation, epithelial-to-mesenchymal transition, angiogenesis, degradation, and remodeling of extracellular matrix. HIF-1α induced by hypoxia or apoplexy inside the adenoma might be the initiating factor of invasive transformation, followed with angiogenesis for overexpressed VEGF, EMT for overexpressed PTTG, degradation of ECM for overexpressed MMPs, creating a suitable microenvironment within the tumor. Together, they form a complex interactive network. More investigations are required to further elucidate the mechanisms underlying the invasiveness of pituitary adenomas.
机译:垂体腺瘤病例占颅内肿瘤的10–25%,是颅内第三大肿瘤,大多数腺瘤被认为是良性的。约35%的垂体腺瘤是浸润性的。这篇综述总结了垂体腺瘤侵袭性的已知分子基础。该研究指出,缺氧诱导因子-1α,垂体肿瘤转化基因,血管内皮生长因子,成纤维细胞生长因子-2和基质金属蛋白酶(MMP,主要是MMP-2和MMP-9)是引起缺氧的核心分子。垂体腺瘤的浸润性。原因是这些分子具有直接或间接诱导细胞增殖,上皮到间质转化,血管生成,降解和细胞外基质重塑的能力。腺瘤内部缺氧或中风引起的HIF-1α可能是浸润性转化的起始因素,其次是血管生成引起过度表达的VEGF,EMT引起过度表达的PTTG,ECM降解导致过度表达的MMP,从而在肿瘤内形成合适的微环境。它们共同构成了一个复杂的交互式网络。需要进一步研究以进一步阐明垂体腺瘤浸润性的潜在机制。

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