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Current clinical development of PI3K pathway inhibitors in glioblastoma

机译:PI3K途径抑制剂在胶质母细胞瘤中的临床研究进展

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摘要

Glioblastoma (GBM) is the most common and lethal primary malignant tumor of the central nervous system, and effective therapeutic options are lacking. The phosphatidylinositol 3-kinase (PI3K) pathway is frequently dysregulated in many human cancers, including GBM. Agents inhibiting PI3K and its effectors have demonstrated preliminary activity in various tumor types and have the potential to change the clinical treatment landscape of patients with solid tumors. In this review, we describe the activation of the PI3K pathway in GBM, explore why inhibition of this pathway may be a compelling therapeutic target for this disease, and provide an update of the data on PI3K inhibitors in clinical trials and from earlier investigation.
机译:胶质母细胞瘤(GBM)是中枢神经系统最常见且致命的原发性恶性肿瘤,缺乏有效的治疗选择。磷脂酰肌醇3-激酶(PI3K)途径在包括GBM在内的许多人类癌症中经常失调。抑制PI3K的药物及其效应物已在多种肿瘤类型中显示出初步的活性,并具有改变实体瘤患者临床治疗前景的潜力。在这篇综述中,我们描述了GBM中PI3K途径的激活,探讨了为什么抑制该途径可能是该疾病的引人注目的治疗靶标,并提供了临床试验和早期研究中PI3K抑制剂的最新数据。

著录项

  • 来源
    《Neuro-Oncology》 |2012年第7期|p.819-829|共11页
  • 作者单位

    Center For Neuro-Oncology, Dana-Farber Cancer Institute, SW430D, 450 Brookline Ave., Boston, MA 02215 Division of Neuro-Oncology, Department of Neurology, Brigham and Women's Hospital Harvard Medical School, Boston, MA;

    Center for Neuro-Oncology, Dana-Farber/Brigham and Women's Cancer Center Division of Neuro-Oncology, Department of Neurology, Brigham and Women's Hospital Harvard Medical School, Boston, MA;

    Harvard Medical School, Boston, MA Center for Neuro-Oncology, Dana-Farber/Brigham and Women's Cancer Center;

    Center for Molecular Oncologic Pathology, Dana-Farber Cancer Institute Department of Pathology, Brigham and Women's Hospital Children's Hospital Boston Harvard Medical School, Boston, MA;

    Division of Neuro-Oncology, MD Anderson Cancer Center, Houston, TX;

  • 收录信息
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

    AKT; glioblastoma; GBM; mtor; PI3K;

    机译:AKT;胶质母细胞瘤GBM;先生PI3K;

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