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排序方式: 共有619条查询结果,搜索用时 15 毫秒
1.
Rupa Narayan MD Traci M. Blonquist MS Ashkan Emadi MD PhD Robert P. Hasserjian MD Meghan Burke BS Christopher Lescinskas BS Donna S. Neuberg ScD Andrew M. Brunner MD Gabriela Hobbs MD Hanno Hock MD PhD Steven L. McAfee MD Yi-Bin Chen MD Eyal Attar MD Timothy A. Graubert MD Christina Bertoli MSN Jenna A. Moran MSN Meghan K. Bergeron MSN Julia E. Foster MSN Aura Y. Ramos BSN Tina T. Som BSN Megan K. Vartanian BSN RN Jennifer L. Story LPN Kristin McGregor MS Molly Macrae BS Tanya Behnan BS Margaret C. Wey PhD Jessica Rae BSN Frederic I. Preffer PhD Patricia Lesho BA Vu H. Duong MD Mason L. Mann BA Karen K. Ballen MD Christine Connolly BS Philip C. Amrein MD Amir T. Fathi MD 《Cancer》2020,126(6):1264-1273
2.
《药学学报(英文版)》2020,10(7):1294-1308
A great challenge in multi-targeting drug discovery is to identify drug-like lead compounds with therapeutic advantages over single target inhibitors and drug combinations. Inspired by our previous efforts in designing antitumor evodiamine derivatives, herein selective histone deacetylase 1 (HDAC1) and topoisomerase 2 (TOP2) dual inhibitors were successfully identified, which showed potent in vitro and in vivo antitumor potency. Particularly, compound 30a was orally active and possessed excellent in vivo antitumor activity in the HCT116 xenograft model (TGI = 75.2%, 150 mg/kg, p.o.) without significant toxicity, which was more potent than HDAC inhibitor vorinostat, TOP inhibitor evodiamine and their combination. Taken together, this study highlights the therapeutic advantages of evodiamine-based HDAC1/TOP2 dual inhibitors and provides valuable leads for the development of novel multi-targeting antitumor agents. 相似文献
3.
ELF方案治疗晚期胃癌21例近期疗效分析 总被引:9,自引:0,他引:9
用ELF(CF/5-Fu及Vp-16)方案治疗均经病理证实的晚期胃癌21例,其中术后辅助性化疗4例,可评价17例,结果CR3例,PR6例,总有效率52.9%,同在存活最活最长30个月,最短3个月,中位生存期9个月,化疗主要毒副作用为轻度骨髓抑制及胃肠道反应,对肝、肾、心功能无大影响。 相似文献
4.
Recently, it has been suggested, that differentiated cells are more resistant to the apoptotic effect of DNA damaging agents
possibly due to the decreased activity of “damage detecting/apoptosis triggering” mechanism. Previously, we have shown, that
PMA pretreatment reduced etoposide-(ETO) but enhanced staurosporine- (STA) -induced apoptosis in HT58 cells. Data presented
here show that the HT58 human, “mature” B-lymphoma cells exposed to PMA secrete more IgM into the supernatant indicating commitment
of cells to perform differentiated function. The sensitivity of HT58 cells to ETO- or STA-induced apoptosis is influenced
diversely with PMA pre- or posttreatment. Interestingly, the DNA damage (gamma radiation, bleomycin, ETO) or okadaic acic
(30 nM) reduced the [PMA+STA] - induced apoptosis. 相似文献
5.
Suramin, a highly sulfonated drug, has been reported to be effective against several human malignancies in vitro and in vivo, and currently is undergoing clinical trials against prostate tumors. The biochemical and molecular mechanisms for suramin's antiproliferative activity are not clear. In order to define the biochemical basis for its antitumor activity and to enhance suramin's chemotherapeutic potential while decreasing its toxicity, we have examined interactions of suramin with topoisomerase I and 11 and several clinically active anticancer drugs against the human prostate (PC3 and LNCaP) cancer cell line. While etoposide, m-AMSA, camptothecin, and SN-38 (the active metabolite of CPT-11) were active in killing prostate cells as single agents, combinations of suramin and these agents were antagonistic against these cells. We found that suramin inhibited activities of purified topoisomerase I and II in vitro as measured by relaxation and cleavage assays. Further studies indicated that suramin also inhibited the drug-induced DNA damage in vitro and in isolated nuclei. These findings indicate that combinations of suramin with topoisomerase inhibitors, for example, VP-16, m-AMSA, or CPT, may not be beneficial to patients receiving suramin-containing chemotherapy. © 1993 Wiley-Liss, Inc. 1 This article is a US Government work and, as such, is in the public domain in the United States of America . 相似文献
6.
Holthuis JJ Römkens FM Pinedo HM van Oort WJ 《Journal of pharmaceutical and biomedical analysis》1983,1(1):89-97
A sensitive high-performance liquid chromatographic (HPLC) assay of the antineoplastic agent VP 16-213 (etoposide) in plasma is described. The system discriminates between the parent compound and possible metabolites, including the aglycone and the cis isomer. After extraction with 1,2-dichloroethane the drugs are chromatographed on a reversed-phase phenyl column with amperometric detection. Quantitative response is linear up to 250 ng/ml for 1 ml human plasma and up to 40.0 mug/ml for 0.1 ml human plasma. The detection limit is ca 2 ng/ml in plasma. Preliminary pharmacokinetic results show that the sensitivity and selectivity of the assay are adequate to establish plasma concentrations over 8-12 half-lives during elimination of the drug. 相似文献
7.
8.
新型抗癌药依托泊苷脂质体的制备 总被引:4,自引:0,他引:4
目的 制备依托泊苷脂质体,测定其含药量及包封率,对其体外释放及原料药的体外释放进行比较,并对脂质体灭菌后的稳定性进行考察。方法 采用薄膜-超声分散法制备依托泊苷脂质体,通过均匀设计优化处方,利用透析法测定其含药量及包封率,进行热压灭菌及60Co灭菌两种灭菌方式,以粒径和包封率为指标考证灭菌后的稳定性。结果 按均匀设计的最优组合制备脂质体的含药量为(574.3±30.7)μg·mL-1,平均包封率为(61.58±0.83)%,依托泊苷脂质体50 h累积释药(96.13±1.11)%,而其原料药3 h累积释药(97.10±1.84)%,热压灭菌的渗漏率比60Co灭菌的渗漏率高。结论 用薄膜-超声分散法制备的依托泊苷脂质体外观圆整,粒径小而均匀,体外释药达到了长效缓释的作用,60Co灭菌后脂质体较稳定。 相似文献
9.
TEP方案治疗小细胞肺癌的临床研究 总被引:5,自引:0,他引:5
目的 :探讨拓扑替康 (topotecan ,TPT )联合依托泊苷 (etoposide ,Vp -16)、顺铂 (cisplatin ,DDP)组成的TEP方案治疗小细胞肺癌的临床疗效、生存期和耐受性。方法 :45例初治SCLC患者 ,其中TEP方案治疗组 2 1例 ,EP方案对照组 2 4例。结果 :TEP组CR 8例 ,PR 8例 ,有效率 (RR)为 76.2 % ,局限期 (LD)者RR为 90 .0 % ,广泛期 (ED)者RR为 63 .6% ,其中 4例脑转移者PR 1例。EP组中CR 7例 ,PR 9例 ,RR为 66.7% ,LD者RR为 81.8% ,ED者RR为 53 .8% ,其中 5例脑转移者未见CR、PR者。两组有效率比较无显著性差异 (P >0 .0 5)。TEP组中位生存期 11.5个月 ,一、二年生存率分别为 42 .9%和 19.0 % ;EP组中位生存期 8.5个月 ,一、二年生存率分别为3 7.5%和 8.3 % ,两组生存期比较 ,差异具有显著性 (P <0 .0 5)。两组主要不良反应为骨髓抑制 ,TEP组Ⅲ~Ⅳ度白细胞减少的发生率 76.2 % (16/ 2 1)明显高于EP组 3 7.5% (9/ 2 4) ,具有统计学意义 (P <0 .0 5) ;两组血小板减少的发生率分别为 61.9%和 3 3 .3 % ,差异显著 (P <0 .0 5)。结论 :TEP方案治疗SCLC疗效肯定 ,可能具有治疗和预防脑转移的作用 ,其生存期及生存率较EP方案均有改善 ,可作为SCLC的一线治疗应用 ;主要不良反应为骨髓抑制 ,临床应用时应予重视 相似文献
10.