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首页> 外文期刊>Modern Pathology >Altered Cellular Distribution of Tuberin and Glucocorticoid Receptor in Sporadic Fundic Gland Polyps
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Altered Cellular Distribution of Tuberin and Glucocorticoid Receptor in Sporadic Fundic Gland Polyps

机译：散发性胃底腺息肉中结核菌素和糖皮质激素受体的细胞分布改变

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Gastric fundic gland polyps (FGPs) are considered hamartomas, and various gastrointestinal hamartomas are associated with tuberous sclerosis complex (TSC). The aim of this study was to investigate a possible link between TSC proteins (hamartin and tuberin) and sporadic FGPs. We examined 33 sporadic FGPs and 26 biopsies of normal fundic mucosa by immunohistochemistry. Nuclear immunoreactivity for tuberin was dramatically reduced or lost in most sporadic FGPs, and tuberin unexpectedly accumulated in the cytoplasm in oxyntic glands. About 18% (6/33) of FGPs were immunopositive in an average of 1.7% of oxyntic cell nuclei, compared with 77% (20/26) of controls in an average of 24.4% of oxyntic cell nuclei (P < .01). No change in hamartin was noted. We further examined the tuberin-associated proteins glucocorticoid receptor (GCR) and p27. Nuclear immunoreactivity for GCR was lost in most sporadic FGPs, but p27 distribution was normal. Sporadic FGPs had a low frequency of staining for Ki-67 except for some cells from cystic components, which is consistent with their slow growth. Our results are consistent with the hypothesis that tuberin may play an important role in pathogenesis of sporadic FGPs. First, an altered cellular localization of tuberin may lead to the deregulation of cell proliferation by interrupting its interaction with hamartin. Second, altered cellular localization of tuberin may preclude its negative regulation of gene transcription mediated by GCR.
机译：胃底腺息肉（FGP）被认为是错构瘤，各种胃肠道错构瘤与结节性硬化症（TSC）相关。这项研究的目的是研究TSC蛋白（哈马汀和结核菌素）与散发的FGP之间的可能联系。我们通过免疫组织化学检查了33例散发性FGP和26例正常胃底黏膜活检。在大多数零星的FGP中，结核菌素的核免疫反应性显着降低或消失，并且结核菌素意外地积聚在含氧腺的细胞质中。约18％（6/33）的FGP在平均1.7％的氧化性细胞核中呈免疫阳性，而对照组的77％（20/26）的对照者在平均24.4％的氧化性细胞核中（P <.01）。没有发现ha素的变化。我们进一步检查了与结核菌素相关的蛋白糖皮质激素受体（GCR）和p27。 GCR的核免疫反应性在大多数零星的FGP中丢失，但p27分布正常。散发的FGP对Ki-67的染色频率较低，除了一些来自囊性成分的细胞外，这与它们的缓慢生长是一致的。我们的结果与以下假设相一致：结核菌素可能在散发性FGP的发病机理中起重要作用。首先，改变了结核菌素的细胞定位可能会通过中断其与ha素的相互作用而导致细胞增殖失调。第二，结核菌素的细胞定位改变可能排除了其对GCR介导的基因转录的负调控。

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