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Mechanism of DNA damage, cell cycle arrest and apoptosis in indolent B-cell lymphomas.

机译：惰性B细胞淋巴瘤的DNA损伤，细胞周期停滞和凋亡机制。

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The disease course of mature B cell lymphoma such as plasma cell and lymphoplasmatic neoplasms are generally indolent, mimicking the low-grade (LG) non-hodgkin's lymphomas. Such LGL and indolent tumors include the chronic lymphocytic leukemia (CLL), Hairy-cell leukemia (HCL), Waldenstrom's macroglobulinemia (WM), and Multiple myeloma (MM). Based on disease progression, response to chemotherapy, and relapse events, LGL and indolent tumors are presently considered unfavorable and incurable with current treatment protocols. The major concern in the treatment of patients with indolent lymphoid malignancies is the problem of relapse (resistant residual cells). Combinations of chemotherapeutic agents have not been successful in irradiating refractory cells. Understanding the mechanism of anti-tumor activity of chemo-therapeutic agents in indolent B-lymphomas, and the responses of these tumors, may explain how residual cells resist the effect of certain chemotherapy drugs. We may then be able to understand the transition indolent cells go through in order to survive, and then target our treatment directly and more effectively.

机译：成熟的B细胞淋巴瘤（如浆细胞和淋巴质性肿瘤）的病程通常是缓慢的，类似于低级（LG）非霍奇金淋巴瘤。此类LGL和惰性肿瘤包括慢性淋巴细胞性白血病（CLL），毛细胞白血病（HCL），华氏巨球蛋白血症（WM）和多发性骨髓瘤（MM）。基于疾病的进展，对化学疗法的反应以及复发事件，目前认为LGL和顽固性肿瘤不利于当前的治疗方案并且无法治愈。惰性淋巴样恶性肿瘤患者治疗的主要问题是复发（耐药性残留细胞）问题。化学疗法的组合在辐射难治性细胞方面尚未成功。了解惰性B淋巴瘤中化学治疗剂的抗肿瘤活性机制以及这些肿瘤的反应，可能可以解释残留细胞如何抵抗某些化学疗法药物的作用。然后，我们也许能够了解惰性细胞为了生存而经历的过渡，然后直接且更有效地靶向我们的治疗。

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作者
Mensah-Osman, Edith Josephine.;
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作者单位

Wayne State University.;

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授予单位 Wayne State University.;
学科 Health Sciences Oncology.; Biology Molecular.
学位 Ph.D.
年度 2003
页码 124 p.
总页数 124
原文格式 PDF
正文语种 eng
中图分类肿瘤学;分子遗传学;
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专利

1. p38 MAPK Activation. DNA Damage,Cell Cycle Arrest and Apoptosis As Mechanisms of Toxichy of Silver Nanoparticles in Jurkat T Cells [J] . HYUN-JEONG EOM, JINHEE CHOI Environmental Science & Technology . 2010,第21期

机译：p38 MAPK激活。 DNA损伤，细胞周期阻滞和凋亡是Jurkat T细胞中银纳米颗粒毒性的机制。
2. Ecotoxicological assessment of cobalt using Hydra model: ROS, oxidative stress, DNA damage, cell cycle arrest, and apoptosis as mechanisms of toxicity [J] . Zeeshan Mohammed, Murugadas Anbazhagan, Ghaskadbi Surendra, Environmental Pollution . 2017,第MAY期

机译：使用Hydra模型对钴进行生态毒理学评估：ROS，氧化应激，DNA损伤，细胞周期停滞和凋亡是毒性机制
3. GM-CSF plus rituximab immunotherapy: translation of biologic mechanisms into therapy for indolent B-cell lymphomas. [J] . Schuster SJ, Venugopal P, Kern JC, Leukemia and lymphoma . 2008,第9期

机译：GM-CSF加利妥昔单抗免疫疗法：将生物学机制转化为惰性B细胞淋巴瘤的疗法。
4. Ugonin K induces Cell Cycle Arrest and Apoptosis through Reactive oxygen species/Apoptosis Signal Pathway in Human Skin Cancer Cells [C] . Leong-Perng Chan, Tzung-Han Chou, Guey-Horng Wang, International Conference on Manufacturing Science and Engineering . 2013

机译：Ugonin K通过在人体皮肤癌细胞中的活性氧物质/凋亡信号途径诱导细胞周期停滞和细胞凋亡
5. Mechanism of 3,3'-diindolylmethane-induced cell death in human C33A cervical cancer cells: Induction of endoplasmic reticulum stress, apoptosis and the role of growth-arrest and DNA-damage genes [D] . Han, Jing Y. 2009

机译：3,3'-二吲哚基甲烷诱导的人C33A宫颈癌细胞死亡的机制：内质网应激，细胞凋亡以及生长停滞和DNA损伤基因的作用
6. Correction: Zhao X.W. et al. Dioscin Induces the Apoptosis of Human Cervical Carcinoma HeLa and SiHa Cells Through ROS-mediated DNA Damage Cell Cycle Arrest and Mitochondrial Signaling Pathways. Molecules 2016 21 730 [O] . Xinwei Zhao, Xufeng Tao, Lina Xu, 2020

机译：校正：ZhaoX.W.等。薯os皂素通过ROS介导的DNA损伤细胞周期阻滞和线粒体信号传导途径诱导人宫颈癌Hela和SiHa细胞凋亡。分子201621730
7. MHY440, a Novel Topoisomerase Ι Inhibitor, Induces Cell Cycle Arrest and Apoptosis via a ROS-Dependent DNA Damage Signaling Pathway in AGS Human Gastric Cancer Cells [O] . Jung Jang, Yong Kang, Bokyung Sung, 2018

机译：MHY440，一种新型拓扑异构酶1抑制剂，通过AGS人胃癌细胞中的ROS依赖性DNA损伤信号通路诱导细胞周期停滞和凋亡
8. Role of GADD34 (Growth Arrest and DNA Damage-Inducible Protein) in Regulating Apoptosis, Proliferation, and Protein Synthesis in Human Breast Cancer Cells [R] . Welser, D. C. 2005

机译：GaDD34（生长抑制和DNa损伤诱导蛋白）在调节人乳腺癌细胞凋亡，增殖和蛋白质合成中的作用

Mechanism of DNA damage, cell cycle arrest and apoptosis in indolent B-cell lymphomas.

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