HCE方案治疗常规方案失效的非小细胞肺癌156例分析

目的：探讨羟基喜树碱（ＨＣＰＴ）、卡铂（ＣＢＰ）和足叶乙甙（ＶＰ－１６）联合治疗常规方案（ＭＶＰ）失效的晚期非小细胞肺癌的疗效。方法：１５６例晚期非小细胞肺癌患者接受常规方案２￣４周期治疗失效后改用ＨＣＰＴ＋ＣＢＴ＋ＶＰ－１６（ＨＣＥ）化疗：ＨＣＰＴ ６ｍｇ／ｍ＾２,ｉｖ,ｄｌ￣５;ＣＢＰ ３００ｍｇ／ｍ＾２,ｉｖ,ｄｌ;ＶＰ－１６ １００ｍｇ,ｉｖ,ｄｌ￣５。２８天为１周期,每例用药２周期。观察     

强化疗加G-CSF对急性髓细胞白血病治疗转归的影响

目的观察强化疗加重组集落刺激因子对急性髓细胞白血病治疗转归的影响。方法诱导化疗采用ＤＮＲ每日４５ｍｇ／ｍ２,静脉注射,第１天～第３天,Ａｒａ－Ｃ每日２００ｍｇ／ｍ２,静脉点滴,第１天～第７天。化疗后白细胞计数（ＷＢＣ）＜１．０×１０９／Ｌ时起加用Ｇ－ＣＳＦ,剂量为每日２００μｇ／ｍ２,皮下注射,直至ＷＢＣ计数＞３．０×１０９／Ｌ或中性粒细胞绝对值（ＡＮＣ）＞１．５×１０９／Ｌ后停用。初治急性髓细胞白血病（ＡＭＬ）１５例。结果完全缓解（ＣＲ）１２例,ＣＲ率８０％,ＰＲ１例,总有效率８６．６％,无治疗相关性死亡。治疗中未发现Ｇ－ＣＳＦ的明显副作用。对ＣＲ１２例进行了连续１２个月的随访,失访２例,持续ＣＲ（ＣＣＲ）７例,复发３例。复发者中２例于ＣＲ后不久中断治疗３个月和４个月后复发,另１例治疗４疗程后于治疗中复发。结论ＡＭＬ强化疗中加用Ｇ－ＣＳＦ对ＣＲ率无影响,而且不增加近期复发率     

强化疗加G—CSF对急性髓细胞白血病治疗转归的影响

观察强化疗加重组集落刺激因子对急性髓细胞白血病治疗转归的影响。方法诱导化疗采用ＤＮＲ每日４５ｍｇ／ｍ＾２，静脉注射，第１天－第３天，Ａｒａ－Ｃ每日２００ｍｇ／ｍ＾２，静脉点滴第１天－第７天。结论ＡＭＬ强化疗中加用Ｇ－ＣＳＦ对ＣＲ率无影响，而且不增加近期复发率。     

长春花碱酰胺联合化疗治疗非霍奇金淋巴瘤35例临床观察

目的：观察长春花碱酰胺（ＶＤＳ）组成的联合方案治疗非霍奇金淋巴瘤（ＮＨＬ）的疗效及毒副反应。方法：３５例ＮＨＬ用以下方案化疗：ＣＴＸ５００ｍｇ／ｍ＾２，ｉｖ，第１、８天；ＡＤＭ３０￣４０ｍｇ／ｍ＾２，ｉｖ，第１天；ＶＤＳ２．５￣３ｍｇ／ｍ＾２，ｉｖ，第１、８天；ＰＤＮ１００ｍｇ／日，ｐｏ，第１至５天，２１￣２８天为１周期。人武部病例用药均在２周期以上。结果：全组３５例，ＣＲ９列，ＰＲ２２例，总有效     

CCAV 与 EP 方案交替应用治疗小细胞肺癌疗效观察

目的：探讨 Ｃ Ｃ Ａ Ｖ 与 Ｅ Ｐ 方案交替应用治疗小细胞肺癌的临床疗效。方法：４２ 例小细胞肺癌,局限期１２ 例,广泛期３０ 例。 Ｃ Ｃ Ａ Ｖ 方案： Ｃ Ｃ Ｎ Ｕ １００ ｍｇ／ｍ ２ ,ｄ１ ,口服; Ｖ Ｃ Ｒ １ ．４ｍｇ／ｍ ２ ,ｄ２ 、９ ,静脉推注; Ｃ Ｔ Ｘ６００ｍｇ／ｍ ２ ,ｄ３ 、１０ ,静脉推注; Ａ Ｄ Ｍ ４０ｍｇ／ｍ ２ ,ｄ３ ,静脉推注。 Ｅ Ｐ 方案： Ｖ Ｐ１６ １００ｍｇ／ｍ ２ ,ｄｌ ～５ ,静滴; Ｄ Ｄ Ｐ２５ｍｇ／ｍ ２ ,ｄｌ ～３ 静滴。两方案每３ ～４ 周交替使用。结果：总有效率（ Ｃ Ｒ＋ Ｐ Ｒ）７３ ．７ ％ ,其中 Ｃ Ｒ１２例, Ｐ Ｒ１９ 例,１ 、２ 、３ 年生存率分别为５７ ．１ ％ 、１６ ．７ ％ 、４ ．８ ％ ,主要不良反应为骨髓抑制、恶心呕吐,病人多可耐受。结论：该治疗方法效果较满意,可推荐应用。     

榄香烯乳加联合化疗治疗难治性急性非淋巴细胞白血病

目的：评价榄香烯乳加联合化疗治疗难治性急性非淋巴细胞白血病。方法：将３０ 例白血病患者随机分为治疗组：用榄香烯乳３００ｍｇ 入５ ％ Ｇ．Ｓ５００ｍｌ 中静脉滴注,持续用药１４ 天,同时用联合化疗：Ａｒａ－ Ｃ０．５ｇ／ｍ２．ｄ ,第１～７ 天;ＶＰ－ １６ １００ｍｇ／ｍ２．ｄ ,第１ ～３ 天;对照组单用联合化疗,方案用量用法同治疗组。结果：治疗组总有效率７７．８ ％ ,对照组总有效率５０ ％ ,差异有显著性（ Ｐ＜ ０．０５）。结论：榄香烯乳对难治性急性非淋巴细胞白血病（ＡＮＬＬ）有肯定疗效,比单用联合化疗效果好,且不良反应少,无血象和骨髓抑制。     

局部晚期乳腺癌新辅助化疗每周方案与三周方案疗效分析

目的　探讨比较局部晚期乳腺癌采用剂量密集法和非剂量密集法行新辅助化疗的近期疗效。方法　４５例ⅢＡ期乳腺癌患者随机进入密集化疗组（Ａ组）和非密集化疗组（Ｂ组）。Ａ组：紫杉醇７０ｍｇ／ｍ^２,表阿霉素３０ｍｇ／ｍ^２,每周１次,连用３周,４周为１个周期。Ｂ组：紫杉醇１３５ｍｇ／ｍ２,第１天,表阿霉素８０ｍｇ／ｍ^２,第１天,３周为１个周期。如无疾病进展,共治疗３个周期。结果　Ａ组获ＣＲ７例（３１.８２％）,ＰＲ1２例（５４.５４％）,ＳＤ３例（１３.６４％）,ｐＣＲ５例（２２.７３％）,有效率（ＲＲ）为８６.３６％。Ｂ组获ＣＲ６例（２６.０９％）,ＰＲ１１例（５０％）,ＳＤ６例（２６.０９％）,ｐＣＲ３例（１３.０４％）,ＲＲ为７３.９１％。Ａ组的ＲＲ、ＣＲ、ｐＣＲ均优于Ｂ组,但无统计学意义。进一步分层分析,不同基因型乳腺癌新辅助化疗的疗效相当,无论Ａ组或Ｂ组,其ＩｕｍｉｎａｌＢ型、Ｂａｓａｌ-ｌｉｋｅ型和ＨＥＲ ２阳性型三者之间新辅助化疗的ＲＲ、ｃＣＲ、ＰＲ、ｐＣＲ的差别无统计学意义。两组３～４级毒副反应发生率除中性粒细胞减少外均相近。两组随访期间全部存活,ＯＳ正在进一步随访中。结论　紫杉类每周方案与标准的三周方案相比,可作用于不同增殖动力学的肿瘤细胞,剂量密度增加,更易于与其他化疗药物配伍,且每周方案较三周方案有更高的疗效,急性毒性无明显增加。     

脐血辅助MxAE方案治疗难治性急非淋白血病临床观察

目的：探讨脐血联合ＭｘＡＥ方案治疗难治性急非淋白血病的效果。方法：脐血联合ＭｘＡＥ方案治疗难治性急非淋白血病２１例,难治笥１４例,复发性７例。治疗方案：米托蒽醌（Ｍｘ）１０ｍｇ／ｄ、１ｄ～３ｄ;阿糖胞苷（Ａｒａ－Ｃ）１５０ｍｇ／ｄ,１ｄ～７ｄ;足叶乙式＊（ＶＰ１６）１００ｍｇ／ｄ,１ｄ～５ｄ。３种药物均静滴,３ｄ～７ｄ业疗程。化疗第１周、第２周输脐因,每周３个～５个单位。结果：完全缓解率（ＣＲ）６     

老年人急性非淋巴细胞白血病化疗疗效观察

报道了五年间收治的老年急性非淋巴细胞白血病（ＡＮＬＬ）２１例，采用ＤＡ（ＶＰ１６）与ＨＡ（ＶＰ１６）联合化疗，依据不同剂量，将其分为二组，二组总有效率为６６．６％。其中中等剂量组１４例，８例ＣＲ，平均生存时间为２６７天；２例（１８％）ＰＲ：小剂量组７例，２例（２８．５％）ＣＲ，２例（２８．５％）ＰＲ；结果提示：对老年白血病患者治疗应个体化，一般情况好者应在强有力支持治疗情况下采用中等剂量的化疗，相反宜小剂量化疗     

联合去甲氧柔红霉素治疗急性白血病的临床研究

采用以４－去甲氧基柔红霉素（ＩＤＡ）为主组成的联合化疗方案，治疗３３例初发和复发的急性白血病，其中急性淋巴细胞白血病（ＡＬＬ）７例，急性非淋巴细胞白血病（ＡＮＬＬ）２６例。结果：总有效率７０％。初治２３例ＡＮＬＬ患者，完全缓解（ＣＲ）１６例，部分缓解（ＰＲ）２例，有效率为７９％。５例初治ＡＬＬ患者，４例ＣＲ，１例ＰＲ。而复发的２例ＡＬＬ和３例ＡＮＬＬ患者均未缓解。ＩＤＡ主要副作用表现为骨髓抑制及心脏毒性。认为以ＩＤＡ组成联合化疗方案治疗初发的急性白血病具有较好的疗效     

Antitumor effects of three platinum complexes, (-)-(R)-2-aminomethylpyrrolidine(1,1-cyclobutanedicarboxylato)-platinum (II) monohydrate (DWA2114R), cis-diammine-(1,1-cyclobutanedicarboxylato)platinum(II) (CBDCA) and cis-diamminedichloroplatinum(II) (CDDP), in mice.

(-)-(R)-2-Aminomethylpyrrolidine(1,1-cyclobutanedicarboxylato++ +)platinum(II) monohydrate (DWA2114R), cis-diammine(1,1-cyclobutanedicarboxylato)platinum(II) (CBDCA) and cis-diamminedichloroplatinum(II) (CDDP) were compared for their antitumor effects and nephrotoxicity-inducing activities at the same dosage (1/8, 1/4, 1/3, 1/2, 2/3 or 3/4 of the LD10 or LD10) on the basis of their intravenous lethal doses in mice. DWA2114R was effective against murine tumor lines, Colon 26 and Colon 38 carcinomas, M5076 ovarian sarcoma and P388 L1210 leukemias, implanted subcutaneously (s.c.). Triple injection every other day of DWA2114R was more effective than a single injection at each sublethal dose. The antitumor effects of DWA2114R against these tumors were more effective than or were similar to those of CBDCA and CDDP. The antitumor effect against CDDP-resistant L1210 leukemia implanted s.c. was only observed in the treatment of DWA2114R, but not in CBDCA and CDDP. No excellent antitumor effects of three platinum complexes were observed against Lewis lung carcinoma and B16 melanoma implanted s.c. even at triple injection every other day, and no effect was obtained against Meth-A fibrosarcoma under similar conditions. While the treatment of CDDP showed marked increases in levels of blood urea nitrogen and of urinary protein and sugar at effective doses in the antitumor evaluations, the treatment of DWA2114R as well as CBDCA showed no increase in these parameters. These results indicate that DWA2114R represents a desirable second generation antitumor platinum complex.     

Clinical trials of Herceptin(R) (trastuzumab)

This report summarises the clinical efficacy and safety findings from clinical trials of the new anti-HER2 monoclonal antibody Herceptin(R) (trastuzumab). Data from pivotal trials indicate that trastuzumab is active when added to chemotherapy in patients with advanced metastatic breast cancer. In particular, the combination significantly prolonged the median time to disease progression, increased the overall response rate, increased the duration of response, and improved median survival time by approximately 25% compared with chemotherapy alone. Furthermore, trastuzumab is active as a single agent in women with HER2-positive metastatic breast cancer, inducing durable objective tumour responses. In total, 15% of patients who had received extensive prior treatment for metastatic disease had an objective response. The median duration of response was 9.1 months following administration of single-agent trastuzumab. Notably, 2% of patients were free of disease progression at 6 months. The safety profile of trastuzumab either given alone or in combination was favourable.     

Synergism of cytotoxicity between cis-diaminedichloro-platinum-(ii) and cis-diamine(1,1-cyclobutanedicarboxylate)-platinum-(ii)

In an attempts to increase the antitumor effect and to reduce normal tissue toxicity, the combined cytotoxic effect of cis-Diamminedichloroplatinum (II) (CDDP) and cis-diammine(1,1-cyclobutane dicarboxylate) platinum (II) (CBDCA) was investigated using HeLa and colon 26 cell lines and the combination index (CI). Cytotoxicity of the combination of CDDP and CBDCA on 27 surgically resected specimens of human gastric and colorectal adenocarcinomas was also evaluated using the in vitro succinate dehydrogenase inhibition (SDI) test. The CI values varied with the dose ratio examined (1:1-1:6) of CDDP and CBDCA, with findings that CI<1, synergy, was obtained at fraction affected (Fa)>0.75 for HeLa cells and at Fa<0.9 for colon 26 cells in cases of a dose ratio of 1:1 to 1:2. Of all 27 clinical human adenocarcinomas, the succinate dehydrogenase (SD) activity was significantly lower in cancer cells concomitantly exposed to both CDDP and CBDCA than in those exposed to either drug alone. These positive effects of a combination of two platinum analogues on human malignant tissues have heretofore not been reported, which would warrant the clinical application of this combination for human malignant tumors.     

In vitro evaluation of dichloro-bis(pyrazole)palladium(II) and dichloro-bis(pyrazole)platinum(II) complexes as anticancer agents

Introduction  Cisplatin (cis-diamminedichloroplatinum) was first identified for its anti-bacterial activity, and was later also shown to be an efficient anticancer agent. However, the therapeutic use of this anticancer drug is somewhat limited by its toxic side effects, which include nephrotoxicity, nausea, and vomiting. Furthermore the development of drug-resistant tumours is commonly observed following therapy with cisplatin. Hence there is a need for improved platinum derived drugs to overcome these limitations. Aims  Apoptosis contributes significantly to the cytotoxic effects of anticancer agents such as cisplatin; therefore in this study the potential anticancer properties of a series of pyrazole palladium(II) and platinum(II) complexes, [(3,5-R₂pz)₂PdCl₂] {R = H (1), R = Me (2)} and [(3,5-R₂pz)₂PtCl₂] {R = H (3), R = Me (4)}, were evaluated by assessment of their pro-apoptotic activity. Methods  The induction of apoptosis was measured in CHO cells by the detection of phosphatidylserine (PS) exposure using the annexin V and APOPercentage™ assays; DNA fragmentation using the Terminal deoxynucleotide transferase dUTP Nick End Labelling (TUNEL) assay; and the detection of activated caspase-3. Results  The platinum complexes were shown to be considerably more active than the palladium complexes, with complex 3 demonstrating the highest level of cytotoxic and pro-apoptotic activity. The LD₅₀ values for complex 3 and cisplatin were 20 and 70 μM, respectively, demonstrating that the cytotoxic activity for complex 3 was three times higher than for cisplatin. Various human cancer cell lines, including CaSki, HeLa, as well as the p53 mutant Jurkat T cell line were also shown to be susceptible to complex 3. Conclusions  Collectively, this in vitro study provides insights into action of palladium and platinum complexes and demonstrates the potential use of these compounds, and in particular complex 3, in the development of new anticancer agents.