肿瘤多药耐药治疗措施研究进展

多药耐药（MDR）是肿瘤化疗失败的主要原因，逆转MDR是目前研究的热点。从逆转剂的应用、MDR的基因治疗、特殊给药载体的介导、MDR的免疫学治疗及影响口服抗癌药物代谢途径等方面对目前国内外MDR治疗措施加以综述。     

肿瘤多药耐药的研究进展

肿瘤临床治疗失败最主要的原因之一就是发生肿瘤细胞的多药耐药(Multidrug resistance,MDR).     

肿瘤多药耐药机制及逆转耐药研究进展北大核心

癌症化学治疗被视为旨在最小化和延迟肿瘤的发生、发展或复发的策略,但是肿瘤多药耐药是肿瘤患者治疗失败和复发的主要原因,是实现肿瘤患者治愈的主要限制因素。如何逆转化疗药物的耐药及耐药机制的研究成为肿瘤研究的挑战。为了解决肿瘤多药耐药问题,本文对传统化疗药物发生肿瘤多药耐药的机制、靶向治疗发生多药耐药的机制以及免疫治疗发生多药耐药的机制进行阐述;确定了癌症耐药性的实验室方法,如MTT测试法、药物敏感性测试、多药耐药基因和途径检测、高通量筛选技术、基因芯片技术等,为多药耐药的研究提供实验方法;并对多药耐药抑制剂或逆转剂的研究进展进行简单的综述,旨在为进一步发明逆转肿瘤多药耐药的药物提供研究基础。     

胰腺癌化疗多药耐药研究进展

胰腺癌的化疗效果不理想主要原因与肿瘤细胞的多药耐药有关。胰腺癌细胞多药耐药产生的机制目前并未阐明,随着对多药耐药认识的不断深入,新的逆转剂已经产生。本文通过近5年文献资料的回顾复习,对胰腺癌耐药机制及其逆转剂的研究进展作一综述。     

肿瘤的多药耐药及耐药逆转剂研究

目前 ,尽管不断有新的化疗药物和化疗方案推出 ,但肿瘤细胞对多种化疗药物产生的多药耐药性(ｍｕｌｔｉｄｒｕｇｒｅｓｉｓｔａｎｃｅ ,ＭＤＲ)仍是化疗失败的主要原因。所谓ＭＤＲ系指肿瘤对一种抗肿瘤药物出现耐药的同时 ,对其他许多结构各异、作用机制不同的抗肿瘤药物亦产生交叉耐药现象。ＭＤＲ现象可以原发性和继发性两种形式出现。原发性 (ｐｒｉｍａｒｙｒｅｓｉｓ ｔａｎｃｅ)是肿瘤细胞固有的对化疗药物不敏感 ,故首次使用化疗药物就产生耐药 ;继发性 (ｓｅｃｏｎｄａｒｙｒｅ ｓｉｓｔａｎｃｅ)则是初始对化疗药物敏感 ,但经过几…     

肝癌多药耐药中药逆转剂的研究进展

多药耐药(MDR)是肿瘤化疗失败的主要原因,寻找高效、低毒的肝癌逆转剂已成为肝癌治疗领域的研究热点,现就中医药在逆转肝癌MDR方面的研究进展作一综述.     

肿瘤的造血干细胞多药耐药基因治疗研究进展

造血干细胞具有多系分化潜能及自我更新能力，其生命周期长，是基因转移的理想靶细胞。这种转基因的造血干细胞可在造血组织中长期稳定表达目的产物，而较成熟的祖细胞作为靶细胞时其基因表达相对短暂。将多药耐药（ＭＤＲ１）基因转移至造血干细胞，在体内存在抗癌药物时具有选择优势，可提高化疗剂量，保护骨髓不受高剂量化疗药物损伤。本文从以下几个方面综述造血干细胞ＭＤＲ基因疗法的原理、临床应用方案及其前景。     

胃肠道肿瘤化疗多药耐药的研究进展

胃肠道肿瘤的治疗是以手术为主,辅以化疗等综合治疗,而往往在有明显症状之前已出现转移,故多数失去手术机会,而选择以化疗为主的综合治疗。然而因肿瘤的原发或继发性对化疗药物的不敏感而导致的多药耐药（MDR）常常影响化疗效果,这是临床常见难题。MDR的机制复杂,现综述胃肠道肿瘤MDR产生的机制以及逆转MDR的策略,将对进一步提高化疗效果具有重要意义。     

肿瘤细胞多药耐药的基础和临床研究进展

 影响肿瘤化疗效果进一步提高的因素很多 ,其中 ,耐药性是影响疗效的最重要的因素之一。肿瘤细胞耐药性的机制概括有以下几点 :①药物的转运或摄取障碍。②药物的活化障碍。③靶酶质和量的改变。④增加利用内替的代谢途径。⑤分解酶增加。⑥修复机制增加。⑦由于特殊的膜糖蛋白的增加 ,而使细胞排出药物增多。⑧DNA链间或链内交联减少。⑨激素受体减少或功能丧失。肿瘤细胞耐药性分为内在性 (未接触药物时原已存在 )和获得性 (接触药物后产生的 )两大类。一般来说 ,对一种肿瘤药物产生耐药性 ,可能会对结构和功能相似的药物产生交叉耐药性 ,但对其他非同类型的药物则仍敏感。近年发现培养中接触某种化疗药物而产生的耐药的细胞株 ,对其他结构和机制不同的药物也产生了耐药性 ,称为多药耐药 (multidrugresis tance ,MDR)。     

Multidrug resistance in prostate cancer

Advanced hormone-refractory prostate cancer remains a therapeutic challenge, because all available pharmaceutical concepts have been ineffective in improving cancer-specific survival. Failure of chemotherapy may be caused by multidrug resistance (MDR) mechanisms protecting cancer cells against cytotoxic drugs, and the question arises whether prostate cancer is also using MDR principles resulting in resistance against chemotherapeutic agents. In consequence, an array of diverse pathways known to lead to MDR such as MDR1, MRPs, glutathione, and apoptosis have been examined and partially established at varying degrees in hormone-refractory prostate cancer. Thus, evidence keeps accumulating for the involvement of some MDR mechanisms in the chemoresistance of prostate cancer in vitro and in vivo. For some of them, e.g. MRP1, functional expression appears to be probable. This lends credit to the idea that reversal, circumvention, or overcoming of MDR pathways in advanced prostate cancer may be feasible and will lead to new avenues with improved treatment efficacy in otherwise intractable disease.     

Multidrug resistance in human cancer

Resistance to cytotoxic chemotherapy continues to be a major obstacle to more effective treatment of human cancers. A particular problem in clinical cancer chemotherapy is the phenomenon of simultaneous resistance of cancers to a variety of unrelated cytotoxic agents. Such resistance to multiple drugs is observed much more often than resistance to individual compounds. A similar experimental phenomenon has been termed multidrug resistance or MDR. Much has been learned in recent years about molecular mechanisms which can lead to MDR in cancer cells and a number of studies has been performed to evaluate the clinical relevance of such mechanisms. In particular, P-glycoprotein-associated MDR (MDR1) has received a lot of attention. This review will discuss (i) some principal aspects of drug resistance in cancer with particular emphasis on MDR1; (ii) available data on drug resistance mechanisms in brain tumors; and (iii) our current knowledge on the putative role of P-glycoprotein in the blood-brain barrier.     

胃癌多药耐药相关机制

Multidrug resistance (MDR) is the main cause of chemotherapy failure. MDR of gastric cancer is associated with a number of factors, including over-expression of P-glycoprotein (P-gp) and MDR associated protein (MRP), ghtathione S-transferase-π(GST-π) activity increasing, topoisomerase Ⅱ(Topo Ⅱ) decreasing and DNA damage-repair ability enhancement.     

胃癌多药耐药相关机制

Multidrug resistance (MDR) is the main cause of chemotherapy failure. MDR of gastric cancer is associated with a number of factors, including over-expression of P-glycoprotein (P-gp) and MDR associated protein (MRP), ghtathione S-transferase-π(GST-π) activity increasing, topoisomerase Ⅱ(Topo Ⅱ) decreasing and DNA damage-repair ability enhancement.     

胃癌多药耐药相关机制

Multidrug resistance (MDR) is the main cause of chemotherapy failure. MDR of gastric cancer is associated with a number of factors, including over-expression of P-glycoprotein (P-gp) and MDR associated protein (MRP), ghtathione S-transferase-π(GST-π) activity increasing, topoisomerase Ⅱ(Topo Ⅱ) decreasing and DNA damage-repair ability enhancement.     

胃癌多药耐药相关机制

Multidrug resistance (MDR) is the main cause of chemotherapy failure. MDR of gastric cancer is associated with a number of factors, including over-expression of P-glycoprotein (P-gp) and MDR associated protein (MRP), ghtathione S-transferase-π(GST-π) activity increasing, topoisomerase Ⅱ(Topo Ⅱ) decreasing and DNA damage-repair ability enhancement.     

胃癌多药耐药相关机制

多药耐药(MDR)是导致胃癌化疗失败的主要原因.研究表明,胃癌MDR的发生机制与多个因素相关,主要有P-糖蛋白(P-gp)和多药耐药相关蛋白(MRP)过表达、谷胱甘肽转移酶-π(GST-π)活性增强、拓扑异构酶Ⅱ(TopoⅡ)含量减少、DNA损伤修复能力增强.     

胃癌多药耐药相关机制

Multidrug resistance (MDR) is the main cause of chemotherapy failure. MDR of gastric cancer is associated with a number of factors, including over-expression of P-glycoprotein (P-gp) and MDR associated protein (MRP), ghtathione S-transferase-π(GST-π) activity increasing, topoisomerase Ⅱ(Topo Ⅱ) decreasing and DNA damage-repair ability enhancement.     

胃癌多药耐药相关机制

Multidrug resistance (MDR) is the main cause of chemotherapy failure. MDR of gastric cancer is associated with a number of factors, including over-expression of P-glycoprotein (P-gp) and MDR associated protein (MRP), ghtathione S-transferase-π(GST-π) activity increasing, topoisomerase Ⅱ(Topo Ⅱ) decreasing and DNA damage-repair ability enhancement.