PTEN and p27 expression in mature T-cell and NK-cell neoplasms

PTEN and p27 expression in mature T-cell and NK-cell neoplasms
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成熟 T 细胞和 NK 细胞肿瘤中 PTEN 和 p27 的表达

DOI:
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发表时间:
2005
影响因子:
2.6
通讯作者:
S. Ruacan
S. Ruacan
中科院分区:
医学4区
文献类型:
--
作者:
A. Üner;A. Sağlam;Ünsal Han;M. Hayran;A. Sungur;S. Ruacan

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PTEN 是一种肿瘤抑制基因,位于染色体 10q23 上,是人类癌症中最常见的突变基因之一。 Pten 的脂质磷酸酶活性使其能够使 PIP3 去磷酸化,从而拮抗由 AKT/PKB 介导的生长因子刺激的 PI3 激酶信号传导。 PTEN 的生长抑制作用已被证明是由 p27 介导的,p27 是 AKT 途径下游的重要效应分子之一。最近,Pten 和 AKT 通路在免疫系统调节和血液恶性肿瘤发展中的重要性已被证实。对 45 名外周 T 细胞和 NK 细胞淋巴瘤患者进行免疫组织化学检查,检测 Pten 和 p27 表达的缺失。在 66.7% 的间变性大细胞淋巴瘤 (ALCL) 病例中检测到 Pten 部分或完全缺失,而在所有其他成熟 T 细胞/NK 细胞淋巴瘤中,这一比例仅为 12.5%。 64.9% 的病例发现 p27 缺失,这与 Pten 缺失呈正相关。在这项研究中,我们发现与其他成熟 T/NK 细胞淋巴瘤相比,ALCL 中 Pten 缺失更为常见,这与 p27 表达缺失密切相关。我们的研究结果为 ALCL 中 PI3K-AKT 通路失调的重要性提供了进一步的证据。
PTEN is a tumor suppressor gene located on chromosome 10q23 and is amongst the most commonly mutated genes in human cancers. The lipid phosphatase activity of Pten enables it to dephosphorylate PIP3, thereby antagonizing growth factor stimulated PI3-kinase signaling mediated by AKT/PKB. The growth inhibition effect of PTEN has been shown to be mediated by p27 which is one of the important effector molecules downstream of the AKT pathway. Recently the importance of the Pten and AKT pathway in the regulation of the immune system and development of hematological malignancies has been shown. Loss of Pten and p27 expressions were examined immunohistochemically in 45 patients with peripheral T- and NK-cell lymphoma. Partial or complete loss of Pten was detected in 66.7% of the cases of anaplastic large cell lymphoma (ALCL) compared to only 12.5% of all other mature T-/NK-cell lymphomas combined. Loss of p27 was identified in 64.9% of cases, which showed a positive correlation with Pten loss. In this study, we showed that loss of Pten is more frequent in ALCL as compared to other mature T-/NK-cell lymphomas, which strongly correlates with the loss of p27 expression. Our findings provide further evidence for the importance of the deregulation of the PI3K-AKT pathway in ALCL.
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