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1
Use of ribozymes and antisense oligodeoxynucleotides to investigate mechanisms of drug resistance.利用核酶和反义寡脱氧核苷酸研究耐药机制。
Cytotechnology. 1998 Sep;27(1-3):113-36. doi: 10.1023/A:1008052401952.
2
The means to an end of tumor cell resistance to chemotherapeutic drugs targeting thymidylate synthase: shoot the messenger.针对胸苷酸合成酶的化疗药物的肿瘤细胞耐药性的解决方法:杀死信使。
Curr Drug Targets. 2002 Aug;3(4):297-309. doi: 10.2174/1389450023347605.
3
Anticancer Drug Development: The Way Forward.抗癌药物研发:前进之路
Oncologist. 1996;1(3):180-181.
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Advances in the development of ribozymes and antisense oligodeoxynucleotides as antiviral agents for human papillomaviruses.作为人乳头瘤病毒抗病毒剂的核酶和反义寡脱氧核苷酸开发进展。
Antivir Ther. 2003 Aug;8(4):265-78.
5
Impact of multicellular resistance on the survival of solid tumors, including micrometastases.多细胞耐药性对实体瘤(包括微转移瘤)存活的影响。
Invasion Metastasis. 1994;14(1-6):50-60.
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Bcl-2 antisense therapy for cancer: the art of persuading tumour cells to commit suicide.
Apoptosis. 1998 Mar;3(2):67-74. doi: 10.1023/a:1009636722713.
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The Challenge of Developing New Therapies for Childhood Cancers.开发儿童癌症新疗法面临的挑战。
Oncologist. 1997;2(1):I-II.
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Molecular mechanisms for tumour resistance to chemotherapy.肿瘤对化疗耐药的分子机制。
Clin Exp Pharmacol Physiol. 2016 Aug;43(8):723-37. doi: 10.1111/1440-1681.12581.
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Co-transfection of MRP and bcl-2 antisense S-oligodeoxynucleotides reduces drug resistance in cisplatin-resistant lung cancer cells.多药耐药相关蛋白(MRP)与bcl-2反义硫代寡脱氧核苷酸共转染可降低顺铂耐药肺癌细胞的耐药性。
Chin Med J (Engl). 2000 Oct;113(10):957-60.
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Cellular effects of antisense c-myc oligodeoxynucleotides are delivery dependent.反义 c-myc 寡脱氧核苷酸的细胞效应依赖于传递。
Drug Deliv. 1996;3(3):149-54. doi: 10.3109/10717549609029444.

本文引用的文献

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Enhancement of chemotherapeutic drug toxicity to human tumour cells in vitro by a subset of non-steroidal anti-inflammatory drugs (NSAIDs).非甾体抗炎药(NSAIDs)的一个子集在体外增强化疗药物对人肿瘤细胞的毒性。
Eur J Cancer. 1998 Jul;34(8):1250-9. doi: 10.1016/s0959-8049(98)00045-8.
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A good antisense molecule is hard to find.一个好的反义分子很难找到。
Trends Biochem Sci. 1998 Feb;23(2):45-50. doi: 10.1016/s0968-0004(97)01155-9.
3
Development of a hammerhead ribozyme against BCL-2. II. Ribozyme treatment sensitizes hormone-resistant prostate cancer cells to apoptotic agents.针对BCL-2的锤头状核酶的研发。II. 核酶治疗使激素抵抗性前列腺癌细胞对凋亡诱导剂敏感。
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Effects of an inducible anti-sense c-myc gene transfer in a drug-resistant human small-cell-lung-carcinoma cell line.
Int J Cancer. 1997 Nov 14;73(4):544-50. doi: 10.1002/(sici)1097-0215(19971114)73:4<544::aid-ijc15>3.0.co;2-9.
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Cross-resistance of CD95- and drug-induced apoptosis as a consequence of deficient activation of caspases (ICE/Ced-3 proteases).由于半胱天冬酶(ICE/Ced-3蛋白酶)激活不足导致CD95诱导的凋亡和药物诱导的凋亡产生交叉耐药性。
Blood. 1997 Oct 15;90(8):3118-29.
6
Bcl-2 is overexpressed and alters the threshold for apoptosis in a cholangiocarcinoma cell line.Bcl-2在胆管癌细胞系中过表达并改变细胞凋亡阈值。
Hepatology. 1997 Oct;26(4):884-90. doi: 10.1002/hep.510260413.
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Treatment of multidrug-resistant murine leukemia with antisense mdr1 oligodeoxynucleotides.
Biomed Pharmacother. 1997;51(6-7):276-83. doi: 10.1016/S0753-3322(97)83543-3.
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The design of antisense RNA.反义RNA的设计
Antisense Nucleic Acid Drug Dev. 1997 Aug;7(4):439-44. doi: 10.1089/oli.1.1997.7.439.
9
Development of a hammerhead ribozyme against bcl-2. I. Preliminary evaluation of a potential gene therapeutic agent for hormone-refractory human prostate cancer.针对bcl-2的锤头状核酶的开发。I. 一种用于激素难治性人类前列腺癌的潜在基因治疗剂的初步评估。
Prostate. 1997 Sep 1;32(4):246-58. doi: 10.1002/(sici)1097-0045(19970901)32:4<246::aid-pros4>3.0.co;2-h.
10
Inhibition of tumorigenicity in lung adenocarcinoma cells by c-erbB-2 antisense expression.
Int J Cancer. 1997 Aug 7;72(4):631-6. doi: 10.1002/(sici)1097-0215(19970807)72:4<631::aid-ijc14>3.0.co;2-e.

利用核酶和反义寡脱氧核苷酸研究耐药机制。

Use of ribozymes and antisense oligodeoxynucleotides to investigate mechanisms of drug resistance.

机构信息

National Cell and Tissue Culture Centre, Dublin City University, Glasnevin, Dublin 9, Ireland.

出版信息

Cytotechnology. 1998 Sep;27(1-3):113-36. doi: 10.1023/A:1008052401952.

DOI:10.1023/A:1008052401952
PMID:19002787
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3449559/
Abstract

Chemotherapy can cure a number of human cancers but resistance (either intrinsic or acquired) remains a significant problem in many patients and in many types of solid tumour. Combination chemotherapy (using drugs with different cellular targets/mechanisms) was introduced in order to kill cells which had developed resistance to a specific drug, and to allow delivery of a greater total dose of anti-cancer chemicals by combining drugs with different side-effects (Pratt et al., 1994). Nearly all anti-cancer drugs kill tumour cells by activating an endogenous bio-chemical pathway for cell suicide, known as programmed cell death or apoptosis.

摘要

化疗可以治愈许多人类癌症,但在许多患者和许多类型的实体肿瘤中,耐药性(内在或获得性)仍然是一个重大问题。联合化疗(使用具有不同细胞靶点/机制的药物)的引入是为了杀死对特定药物产生耐药性的细胞,并通过结合具有不同副作用的药物来输送更大剂量的抗癌化学物质(Pratt 等人,1994 年)。几乎所有的抗癌药物都是通过激活一种称为程序性细胞死亡或细胞凋亡的内源性细胞自杀生物化学途径来杀死肿瘤细胞的。