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首页> 外文期刊>Journal of Pharmacological and Toxicological Methods >In vitro studies of DNA damage and its repair in cells from NHL patients with different p53 mutant protein status, resistant (p53(+)) and sensitive (p53(-)) to cancer chemotherapy.
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In vitro studies of DNA damage and its repair in cells from NHL patients with different p53 mutant protein status, resistant (p53(+)) and sensitive (p53(-)) to cancer chemotherapy.

机译：具有不同p53突变蛋白状态，对癌症化疗耐药（p53（+））和敏感（p53（-））的NHL患者的细胞中DNA损伤及其修复的体外研究。

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INTRODUCTION: Resistance to an anthracycline-based regimen, such as CHOP, constitutes a problem for curing non-Hodgkin's lymphoma (NHL) patients. Chemoresistance in the clinic manifests itself as a lack of response to treatment or regrowth of a tumour after an initial response. METHODS: In this study, lymphocytes from NHL patients were treated with hydrogen peroxide (H(2)O(2)), a free radical generating model agent, and ethyl methanesulfonate (EMS), a model alkylating agent, to induce DNA damage which was evaluated by SCGE. This study assessed whether or not there were any differences in the patterns of damage and repair between cells from patients with p53 mutant protein abnormalities, i.e. over-expression (p53(+)) not responding to the CHOP regimen and patients responding to the CHOP regimen without p53 protein abnormalities (p53(-)) by comparison with control individuals (wild-type). An NHL cell line model [Raji TK(+) (mex(+)) and TK(-) (mex(-))] with p53 over-expression was also investigated. RESULTS: Results showed that frozen/thawed samples from healthy people were not suitable for use in repair studies, whilst fresh samples or samples incubated for 20 h at room temperature could be used. Tumour cells were more sensitive to damage than control cells. After treatment with H(2)O(2), cells from fresh or incubated blood showed a similar repair capacity. After treatment with EMS, there was a difference between repair in resistant and sensitive cells. DISCUSSION: These results suggest that the repair process is a useful cellular biomarker for investigating chemoresistance. The lack of repair in p53(+) cells may correlate with a low level of MGMT, since there was no repair in the Raji TK(-) cells lacking this enzyme.
机译：简介：对基于蒽环类的方案（例如CHOP）的耐药性构成了治愈非霍奇金淋巴瘤（NHL）患者的问题。临床上的化学抗性表现为在最初的反应后对治疗或肿瘤的再生缺乏反应。方法：在这项研究中，将NHL患者的淋巴细胞用自由基产生模型剂过氧化氢（H（2）O（2））和模型烷基化剂甲磺酸乙酯（EMS）处理，以诱导DNA损伤，由SCGE评估。这项研究评估了p53突变蛋白异常患者（即过表达（p53（+））对CHOP方案无反应）和对CHOP方案有反应的患者之间的细胞损伤和修复模式是否存在差异。与对照个体（野生型）相比，没有p53蛋白异常（p53（-））。还研究了p53过表达的NHL细胞系模型[Raji TK（+）（mex（+））和TK（-）（mex（-））]。结果：结果表明，健康人的冷冻/解冻样品不适合用于修复研究，而新鲜样品或在室温下孵育20小时的样品均可使用。肿瘤细胞比对照细胞对损伤更敏感。用H（2）O（2）处理后，来自新鲜血液或培养的血液的细胞显示出相似的修复能力。用EMS处理后，耐药细胞和敏感细胞的修复之间存在差异。讨论：这些结果表明修复过程是研究化学抗性的有用的细胞生物标志物。由于缺少这种酶的Raji TK（-）细胞没有修复，p53（+）细胞中缺乏修复可能与MGMT水平低有关。

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