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本文引用的文献

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Gemcitabine sensitization by checkpoint kinase 1 inhibition correlates with inhibition of a Rad51 DNA damage response in pancreatic cancer cells.通过抑制检查点激酶1使吉西他滨致敏与抑制胰腺癌细胞中的Rad51 DNA损伤反应相关。
Mol Cancer Ther. 2009 Jan;8(1):45-54. doi: 10.1158/1535-7163.MCT-08-0662.
2
AZD7762, a novel checkpoint kinase inhibitor, drives checkpoint abrogation and potentiates DNA-targeted therapies.新型检查点激酶抑制剂AZD7762可促使检查点消除并增强针对DNA的治疗效果。
Mol Cancer Ther. 2008 Sep;7(9):2955-66. doi: 10.1158/1535-7163.MCT-08-0492.
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The combination of epidermal growth factor receptor inhibitors with gemcitabine and radiation in pancreatic cancer.表皮生长因子受体抑制剂与吉西他滨及放疗联合用于胰腺癌治疗
Clin Cancer Res. 2008 Aug 15;14(16):5142-9. doi: 10.1158/1078-0432.CCR-07-4072.
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Radiotherapy combined with gemcitabine and oxaliplatin in pancreatic cancer cells.放疗联合吉西他滨和顺铂治疗胰腺癌。
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Radiosensitization by gemcitabine fixed-dose-rate infusion versus bolus injection in a pancreatic cancer model.吉西他滨固定剂量率输注与推注在胰腺癌模型中的放射增敏作用。
Transl Oncol. 2008 Mar;1(1):44-9. doi: 10.1593/tlo.07118.
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Survival of cancer cells is maintained by EGFR independent of its kinase activity.癌细胞的存活由表皮生长因子受体(EGFR)维持,且与其激酶活性无关。
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Wild-type KRAS is required for panitumumab efficacy in patients with metastatic colorectal cancer.野生型KRAS是帕尼单抗对转移性结直肠癌患者疗效所必需的。
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The radioprotector Bowman-Birk proteinase inhibitor stimulates DNA repair via epidermal growth factor receptor phosphorylation and nuclear transport.放射防护剂鲍曼-伯克蛋白酶抑制剂通过表皮生长因子受体磷酸化和核转运刺激DNA修复。
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Synthesis and structure-activity relationships of soluble 8-substituted 4-(2-chlorophenyl)-9-hydroxypyrrolo[3,4-c]carbazole-1,3(2H,6H)-diones as inhibitors of the Wee1 and Chk1 checkpoint kinases.可溶性8-取代-4-(2-氯苯基)-9-羟基吡咯并[3,4-c]咔唑-1,3(2H,6H)-二酮作为Wee1和Chk1检查点激酶抑制剂的合成及其构效关系
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10
Randomized crossover study evaluating the effect of gemcitabine infusion dose rate: evidence of auto-induction of gemcitabine accumulation.评估吉西他滨输注剂量率影响的随机交叉研究:吉西他滨蓄积自诱导的证据。
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使用分子靶向治疗提高吉西他滨介导的放射增敏作用:综述

Improving gemcitabine-mediated radiosensitization using molecularly targeted therapy: a review.

作者信息

Morgan Meredith A, Parsels Leslie A, Maybaum Jonathan, Lawrence Theodore S

机构信息

Department of Radiation Oncology, University of Michigan, Ann Arbor, Michigan 48109-5637, USA.

出版信息

Clin Cancer Res. 2008 Nov 1;14(21):6744-50. doi: 10.1158/1078-0432.CCR-08-1032.

DOI:10.1158/1078-0432.CCR-08-1032
PMID:18980967
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2697824/
Abstract

In the last three decades, gemcitabine has progressed from the status of a laboratory cytotoxic drug to a standard clinical chemotherapeutic agent and a potent radiation sensitizer. In an effort to improve the efficacy of gemcitabine, additional chemotherapeutic agents have been combined with gemcitabine (both with and without radiation) but with toxicity proving to be a major limitation. Therefore, the integration of molecularly targeted agents, which potentially produce less toxicity than standard chemotherapy, with gemcitabine radiation is a promising strategy for improving chemoradiation. Two of the most promising targets, described in this review, for improving the efficacy of gemcitabine radiation are epidermal growth factor receptor and checkpoint kinase 1.

摘要

在过去三十年中,吉西他滨已从一种实验室细胞毒性药物发展成为一种标准的临床化疗药物和一种强效的放射增敏剂。为了提高吉西他滨的疗效,已将其他化疗药物与吉西他滨联合使用(无论是否联合放疗),但毒性已被证明是一个主要限制因素。因此,将可能比标准化疗产生更低毒性的分子靶向药物与吉西他滨放疗相结合,是一种有前景的改善放化疗效果的策略。本综述中描述的、用于提高吉西他滨放疗疗效的两个最有前景的靶点是表皮生长因子受体和检查点激酶1。