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系统生物学和放射生物学原理的整合:开发用于优化 IUdR 介导的 DNA 错配修复缺陷(耐受损伤)人类癌症放射增敏的计算模型。

Integration of Principles of Systems Biology and Radiation Biology: Toward Development of in silico Models to Optimize IUdR-Mediated Radiosensitization of DNA Mismatch Repair Deficient (Damage Tolerant) Human Cancers.

机构信息

Department of Radiation Oncology, Warren Alpert Medical School of Brown University and Rhode Island Hospital Providence, RI, USA.

出版信息

Front Oncol. 2011 Aug 10;1:20. doi: 10.3389/fonc.2011.00020. eCollection 2011.

DOI:10.3389/fonc.2011.00020
PMID:22649757
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3355906/
Abstract

Over the last 7 years, we have focused our experimental and computational research efforts on improving our understanding of the biochemical, molecular, and cellular processing of iododeoxyuridine (IUdR) and ionizing radiation (IR) induced DNA base damage by DNA mismatch repair (MMR). These coordinated research efforts, sponsored by the National Cancer Institute Integrative Cancer Biology Program (ICBP), brought together system scientists with expertise in engineering, mathematics, and complex systems theory and translational cancer researchers with expertise in radiation biology. Our overall goal was to begin to develop computational models of IUdR- and/or IR-induced base damage processing by MMR that may provide new clinical strategies to optimize IUdR-mediated radiosensitization in MMR deficient (MMR(-)) "damage tolerant" human cancers. Using multiple scales of experimental testing, ranging from purified protein systems to in vitro (cellular) and to in vivo (human tumor xenografts in athymic mice) models, we have begun to integrate and interpolate these experimental data with hybrid stochastic biochemical models of MMR damage processing and probabilistic cell cycle regulation models through a systems biology approach. In this article, we highlight the results and current status of our integration of radiation biology approaches and computational modeling to enhance IUdR-mediated radiosensitization in MMR(-) damage tolerant cancers.

摘要

在过去的 7 年中,我们专注于实验和计算研究,旨在提高对碘脱氧尿苷(IUdR)和电离辐射(IR)诱导的 DNA 碱基损伤的生化、分子和细胞处理的理解,这些研究由国家癌症研究所综合癌症生物学计划(ICBP)资助,汇集了工程、数学和复杂系统理论方面的系统科学家以及辐射生物学方面的转化癌症研究人员。我们的总体目标是开始开发由 MMR 处理 IUdR 和/或 IR 诱导的碱基损伤的计算模型,这些模型可能为优化 MMR 缺陷(MMR(-))“耐受损伤”人类癌症中的 IUdR 介导的放射增敏作用提供新的临床策略。我们使用多种实验测试尺度,从纯化蛋白系统到体外(细胞)和体内(裸鼠中的人肿瘤异种移植物)模型,开始通过系统生物学方法将这些实验数据与 MMR 损伤处理的混合随机生化模型和概率细胞周期调控模型进行整合和内插。在本文中,我们重点介绍了我们整合放射生物学方法和计算模型以增强 MMR(-)耐受损伤癌症中的 IUdR 介导的放射增敏作用的结果和现状。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d84/3355906/f9b9f6f010ff/fonc-01-00020-g007.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d84/3355906/f9b9f6f010ff/fonc-01-00020-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d84/3355906/a9cce383e9d9/fonc-01-00020-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d84/3355906/75683a8b6077/fonc-01-00020-g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d84/3355906/f9b9f6f010ff/fonc-01-00020-g007.jpg

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The tumor microenvironment and DNA repair.肿瘤微环境与 DNA 修复。
Semin Radiat Oncol. 2010 Oct;20(4):282-7. doi: 10.1016/j.semradonc.2010.05.006.
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Defective mismatch repair as a predictive marker for lack of efficacy of fluorouracil-based adjuvant therapy in colon cancer.错配修复缺陷作为氟尿嘧啶为基础的辅助治疗结肠癌无效的预测标志物。
Medicine (Baltimore). 2019 Jun;98(25):e15721. doi: 10.1097/MD.0000000000015721.
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BNIP3 is essential for mediating 6-thioguanine- and 5-fluorouracil-induced autophagy following DNA mismatch repair processing.BNIP3 对于介导 DNA 错配修复处理后 6-硫代鸟嘌呤和 5-氟尿嘧啶诱导的自噬是必不可少的。
Cell Res. 2010 Jun;20(6):665-75. doi: 10.1038/cr.2010.40. Epub 2010 Apr 6.
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Microsatellite instability predicts clinical outcome in radiation-treated endometrioid endometrial cancer.微卫星不稳定性可预测经放射治疗的子宫内膜样型子宫内膜癌的临床结局。
Int J Radiat Oncol Biol Phys. 2010 Jan 1;76(1):9-13. doi: 10.1016/j.ijrobp.2009.09.035.
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Differential cellular responses to prolonged LDR-IR in MLH1-proficient and MLH1-deficient colorectal cancer HCT116 cells.MLH1 缺陷和野生型结直肠癌细胞 HCT116 对长程 LDR-IR 的差异细胞反应。
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