靶向检查点激酶WEE1：癌细胞对DNA损伤药物的选择性增敏作用 - Suppr

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超能文献

Targeting the checkpoint kinase WEE1: selective sensitization of cancer cells to DNA-damaging drugs.

作者信息

Indovina Paola, Giordano Antonio

机构信息

Department of Human Pathology and Oncology, University of Siena, Siena, Italy.

出版信息

Cancer Biol Ther. 2010 Apr 1;9(7):523-5. doi: 10.4161/cbt.9.7.11276.

DOI:10.4161/cbt.9.7.11276

PMID:20150761

Abstract

摘要

相似文献

Targeting the checkpoint kinase WEE1: selective sensitization of cancer cells to DNA-damaging drugs.靶向检查点激酶WEE1：癌细胞对DNA损伤药物的选择性增敏作用

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Wee1 inhibition can suppress tumor proliferation and sensitize p53 mutant colonic cancer cells to the anticancer effect of irinotecan.Wee1 抑制可以抑制肿瘤增殖，并使 p53 突变型结肠癌细胞对伊立替康的抗癌作用敏感。

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Preclinical evaluation of the WEE1 inhibitor MK-1775 as single-agent anticancer therapy.WEE1 抑制剂 MK-1775 的临床前评估作为单一抗癌疗法。

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Wee1 kinase as a target for cancer therapy.Wee1 激酶作为癌症治疗的靶点。

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Small-molecule inhibition of Wee1 kinase by MK-1775 selectively sensitizes p53-deficient tumor cells to DNA-damaging agents.小分子抑制剂 MK-1775 抑制 Wee1 激酶可选择性增强 p53 缺陷型肿瘤细胞对 DNA 损伤药物的敏感性。

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Abrogating G₂/M checkpoint through WEE1 inhibition in combination with chemotherapy as a promising therapeutic approach for mesothelioma.通过抑制WEE1来消除G₂/M检查点，并联合化疗，作为一种有前景的间皮瘤治疗方法。

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Chk1 inhibition and Wee1 inhibition combine synergistically to impede cellular proliferation.chk1 抑制和 wee1 抑制协同作用以阻碍细胞增殖。

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Targeting AXL and mTOR Pathway Overcomes Primary and Acquired Resistance to WEE1 Inhibition in Small-Cell Lung Cancer.靶向 AXL 和 mTOR 通路克服小细胞肺癌对 WEE1 抑制的原发和获得性耐药。

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Pharmacological Inhibition of WEE1 Potentiates the Antitumoral Effect of the Oncolytic Virus in Malignant Mesothelioma Cell Lines.药物抑制 WEE1 增强溶瘤病毒对恶性间皮瘤细胞系的抗肿瘤作用。

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A Small-Molecule Inhibitor of WEE1, AZD1775, Synergizes with Olaparib by Impairing Homologous Recombination and Enhancing DNA Damage and Apoptosis in Acute Leukemia.小分子 WEE1 抑制剂 AZD1775 通过损伤同源重组并增强 DNA 损伤和细胞凋亡协同奥拉帕利增强急性白血病疗效。

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Cucurbitacin B induced ATM-mediated DNA damage causes G2/M cell cycle arrest in a ROS-dependent manner.葫芦素B诱导的ATM介导的DNA损伤以ROS依赖的方式导致G2/M期细胞周期停滞。

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Simultaneously expressed miR-424 and miR-381 synergistically suppress the proliferation and survival of renal cancer cells---Cdc2 activity is up-regulated by targeting WEE1.同时表达的 miR-424 和 miR-381 协同抑制肾癌细胞的增殖和存活---通过靶向 WEE1 上调 Cdc2 活性。

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