不同铂类联合紫杉类或长春瑞滨对非小细胞肺癌荷瘤裸鼠抑瘤作用的实验研究*

目的　探讨洛铂（ＬＢＰ）、顺铂（ＤＤＰ）和卡铂（Ｃａｂ）单用或联合紫杉醇（ＰＴＸ）、多西他赛（ＤＯＣ）和长春瑞滨（ＮＶＢ）对非小细胞肺癌（ＮＳＣＬＣ）荷瘤裸鼠的抑瘤作用。方法　选用人大细胞肺癌细胞株ＮＣＩ-Ｈ４６０接种于裸小鼠皮下成瘤。单药抑瘤实验中设ＬＢＰ（３.７５、７.５、１５ｍｇ／ｋｇ）３组及Ｃａｂ（６０ｍｇ／ｋｇ）、ＤＤＰ（５ｍｇ／ｋｇ）各１组;联合抑瘤实验设ＬＢＰ（７.５ｍｇ／ｋｇ）、ＤＰＰ（２.５ｍｇ／ｋｇ）分别与ＤＯＣ（５ｍｇ／ｋｇ）、ＰＴＸ（１２ｍｇ／ｋｇ）、ＮＶＢ（５ｍｇ／ｋｇ）联合共６组以及各自单药５组,每组均随机分配６只成瘤小鼠,经静脉ｄ０、ｄ７给药（ＰＴＸｄ０、ｄ２、ｄ４给药除外）。各设１组对照组,每组１２只。每周２～３次记录瘤体体积和裸鼠体重,并计算相对肿瘤增殖率（Ｔ／Ｃ）。结果　（１）单药抑瘤实验中,ＬＢＰ抑瘤效果与剂量相关,中、高剂量组的Ｔ／Ｃ分别为５１.１％和３６.３％,低于Ｃａｂ组（５１.６％）,但ＬＢＰ高剂量组有１只小鼠出现药物相关性死亡。对裸鼠体重的影响由大到小依次为：ＤＤＰ组＞ＬＢＰ高剂量组＞ＬＢＰ中剂量组＞Ｃａｂ组＞ＬＢＰ低剂量组。（２）联合抑瘤实验中,ＬＢＰ＋ＰＴＸ组的Ｔ／Ｃ最低,为２４.4％,明显优于ＤＤＰ＋ＰＴＸ组（Ｐ＜０.０５）;ＬＢＰ＋ＤＯＣ组和ＤＤＰ＋ＤＯＣ组亦对小鼠体重有明显影响。结论　ＬＢＰ单药对ＮＣＩ Ｈ４６０荷瘤小鼠的抑瘤作用呈剂量依赖性,介于ＤＤＰ与Ｃａｂ之间;而ＬＢＰ联合ＰＴＸ的抑瘤作用最强,明显优于ＤＤＰ联合ＰＴＸ及其他两药联合。     

INDEPENDENT AND SYNERGIC INHIBITION OF VERAPAMIL AND ELECTRIC BEAM RADIATION ON CLONOGENIC GROWTH IN K562 AND K562／ADM CELL L

ＩＮＤＥＰＥＮＤＥＮＴＡＮＤＳＹＮＥＲＧＩＣＩＮＨＩＢＩＴＩＯＮＯＦＶＥＲＡＰＡＭＩＬＡＮＤＥＬＥＣＴＲＩＣＢＥＡＭＲＡＤＩＡＴＩＯＮＯＮＣＬＯＮＯＧＥＮＩＣＧＲＯＷＴＨＩＮＫ５６２ＡＮＤＫ５６２／ＡＤＭＣＥＬＬＬＩＮＥＳＩＮＶＩＴＲＯ￥ＸｉｅＺｕｏ...     

PROMOTION OF CHEMICAL CARCINOGENESIS AND P53 EXPRESSION BY REDUCTION OF SUPEROXIDE DISMUTASE ACTIVITY IN THE LUNG OF RAT IN V

ＰＲＯＭＯＴＩＯＮＯＦＣＨＥＭＩＣＡＬＣＡＲＣＩＮＯＧＥＮＥＳＩＳＡＮＤＰ５３ＥＸＰＲＥＳＳＩＯＮＢＹＲＥＤＵＣＴＩＯＮＯＦＳＵＰＥＲＯＸＩＤＥＤＩＳＭＵＴＡＳＥＡＣＴＩＶＩＴＹＩＮＴＨＥＬＵＮＧＯＦＲＡＴＩＮＶＩＶＯ￥ＹｕＬｕｎｙｉｎ；喻伦银；Ｂｉ...     

THE EFFECT OF ACTIVE COMPONENTS OF LYCIUM BARBARUM AND GARLIC（LB－GO）ON THE SYNTHESIS OF DNA AND ULTRASTRUCTURE OF U_（14） CERV

ＴＨＥＥＦＦＥＣＴＯＦＡＣＴＩＶＥＣＯＭＰＯＮＥＮＴＳＯＦＬＹＣＩＵＭＢＡＲＢＡＲＵＭＡＮＤＧＡＲＬＩＣ（ＬＢ－ＧＯ）ＯＮＴＨＥＳＹＮＴＨＥＳＩＳＯＦＤＮＡＡＮＤＵＬＴＲＡＳＴＲＵＣＴＵＲＥＯＦＵ_（１４）ＣＥＲＶＩＸＣＡＮＣＥＲＣＥＬＬＳＩＮＭＩＣ?..     

A MICROCOMPUTER PROGRAM FOR CALCULATINGTHE CONFIDENCE INTERVALS OF SURVIVAL PROBABILITY IN MEDICAL FOLLOW－UP STUDIES

ＡＭＩＣＲＯＣＯＭＰＵＴＥＲＰＲＯＧＲＡＭＦＯＲＣＡＬＣＵＬＡＴＩＮＧＴＨＥＣＯＮＦＩＤＥＮＣＥＩＮＴＥＲＶＡＬＳＯＦＳＵＲＶＩＶＡＬＰＲＯＢＡＢＩＬＩＴＹＩＮＭＥＤＩＣＡＬＦＯＬＬＯＷ－ＵＰＳＴＵＤＩＥＳＸｉａｎｇｙｏｎｇｂｉｎｇ项永兵；Ｇａｏｙｕ...     

去甲长春花碱,异环磷酰胺和顺铂动静脉给药治疗46例非小细？…

目的：观察去甲长春花碱（ＮＶＢ）、异环磷酰胺（ＩＦＯ）和大剂量顺铂（ＤＤＰ）联合动、静脉给药治疗晚期非小细胞肺癌（ＮＳＣＬＣ）的疗效及不良反应。方法：４６例ＮＳＣＬＣ随机分为供瘤动脉给药组（Ａ组）和静脉给药组（Ｂ组）。Ａ组：２６例,ＮＶＢ３０ｍｇ／ｍ＾２,ＤＤＰ８０ｍｇ／ｍ＾２,供瘤支气管动脉灌注,第１天;Ｂ组：２０例,ＮＶＢ３０ｍｇ／ｍ＾２,ＤＤＰ８０ｍｇ／ｍ＾２,静脉点滴,第１天。２组均用ＩＦ     

诺维本联合顺铂治疗NSCLC 90例临床观察

目的 评价诺维本（ｎａｖｅｌｂｉｎｅ,ＮＶＢ）与顺铂（ｃｉｓｐｌａｔｉｎ,ＤＤＰ）联合治疗非小细胞肺癌（ｎｏｎ－ｓｍａｌｌ ｃｅｌｌ ｌｕｎｇ ｃａｎｃｅｒ,ＮＳＣＬＣ）的疗铲及毒副反应。方法 自１９９４年４月至１９９８年１２月对９０例中晚期ＮＳＣＬＣ患者进行ＮＶＢ＋ＤＤＰ联合化疗,第１、８天用ＮＶＢ２５～３０ｍｇ／ｍ＾２,第３天用ＤＤＰ６０～８０ｍｇ／ｍ＾２,每２８天为一周期,每例患者至少完成２     

SERO-EPIDEMIOLOGICAL STUDIES OF EPSTEIN-BARR VIRUS(EBV) INFECTION BY TESTING ANTIBODIES AGAINST EBV SPECIFIC DNASE(EDAb) AS A METHOD FOR EARLY DETECTION OF NASOPHARYNGEAL CARCINOMA(NPC)

ＳＥＲＯＥＰＩＤＥＭＩＯＬＯＧＩＣＡＬＳＴＵＤＩＥＳＯＦＥＰＳＴＥＩＮＢＡＲＲＶＩＲＵＳ（ＥＢＶ）ＩＮＦＥＣＴＩＯＮＢＹＴＥＳＴＩＮＧＡＮＴＩＢＯＤＩＥＳＡＧＡＩＮＳＴＥＢＶＳＰＥＣＩＦＩＣＤＮＡＳＥ（ＥＤＡｂ）ＡＳＡＭＥＴＨＯＤＦＯＲＥＡＲＬＹ...     

肝癌单克隆抗体与氨甲喋呤交联物的制备及细胞毒的研究

在肝癌单克隆抗体Ｈｅｐａｍａ－１－人血清白蛋白－ＭＴＸ结合物的制备中，首先ＭＴＸ在二环己基碳二亚胺（Ｄｉｃｙｃｌｏｈｅｘｙｌｃａｒｂｏｄｉｍｉｄｅ，ＤＣＣ）作用下，与Ｎ－羟基琥珀酰亚胺（Ｎ－Ｈｙｄｒｏｘｙｓｕｃｃｉｎｉｍｉｄｅ，ＮＨＳ）反应，得到ＭＴＸ活性酯，中间载体ＨＳＡ与ＳＰＤＰ作用引入巯基，再与ＭＴＸ活性酯反应得到ＨＳ－ＨＳＡ－ＭＴＸ。然后与碘乙酰化单克隆抗体Ｈｅｐａｍａ－Ｉ反应，获得硫醚键连接的交联物。交联物中Ｈｅｐａｍａ－Ｉ：ＨＳＡ：ＭＴＸ克分子比为１１．６３０，对靶细胞ＢＥＬ－７４０５及对照细胞ＨｅＬａ的杀伤效率，以交联物按ＭＴＸ的克分子浓度计算，ＩＣ５０（５０％抑止率）分别为２．５×１０－８ｍｏｌ／Ｌ和６．４×１０－７ｍｏｌ／Ｌ。单独ＭＴＸ对上述二种细胞株不显示选择性杀伤，ＩＣ５０均为７．１×１０－８ｍｏｌ／Ｌ。     

COMPARATIVE PATHOLOGICAL AND FCM STUDIES ON THE PRIMARY AND METASTATIC CANCERS IN STOMACH AND BREAST

ＣＯＭＰＡＲＡＴＩＶＥＰＡＴＨＯＬＯＧＩＣＡＬＡＮＤＦＣＭＳＴＵＤＩＥＳＯＮＴＨＥＰＲＩＭＡＲＹＡＮＤＭＥＴＡＳＴＡＴＩＣＣＡＮＣＥＲＳＩＮＳＴＯＭＡＣＨＡＮＤＢＲＥＡＳＴ￥ＺｈａｎｇＸｉａｎｇｈｏｎｇ；张祥宏；ＺｈａｎｇＪｉｅｙｉｎｇ；张杰英；Ｘｉ...     

Preclinical Activity of Lobaplatin as a Single Agent and in Combination with Taxanes for Ovarian Carcinoma Cells

Lobaplatin, one of the third - generation platinum compounds, has shown encouraging anticancer activityin a variety of tumor types. However, the efficacy of lobaplatin in ovarian cancer has not been systemicallyevaluated. In this study, lobaplatin as a single agent and in combination with taxanes was investigated in - vitroand in an in vitro model of ovarian carcinoma. Using the sulforhodamine B (SRB) assay, the cytotoxic effects oflobaplatin alone and in combination with taxanes were compared with cisplatin and carboplatin in seven ovariancancer cell lines. In addition, in - vitro antitumor activities were evaluated with cisplatin - sensitive and cisplatin- resistant human ovarian cancer xenografts in nude mice. The cytotoxicity of lobaplatin was similar to or higherthan that of cisplatin and carboplatin, with IC50 values from 0.9 to 13.8 μmol/L in a variety of ovarian cancercells. The combination of lobaplatin with docetaxel yielded enhanced cytotoxic activity in vitro. In addition, inplatinum - sensitive ovarian cancer xenografts, lobaplatin alone showed similar antitumor activity to cisplatinand carboplatin. Furthermore, lobaplatin alone or in combination with docetaxel exhibited significant activityin platinum - resistant ovarian cancer xenografts. These results indicate that the use of lobaplatin alone or incombination with docetaxel might be a rational and novel therapeutic strategy for ovarian cancer. Furtherclinical development of lobaplatin is clearly warranted.     

Potentiation of platinum antitumor effects in human lung tumor xenografts by the angiogenesis inhibitor squalamine: effects on tumor neovascularization.

Squalamine is a novel anti-angiogenic aminosterol that is postulated to inhibit neovascularization by selectively inhibiting the sodium-hydrogen antiporter exchanger. To determine how to most effectively use this agent in patients with cancer, we examined the antitumor effects of squalamine with or without cytotoxic agents in human lung cancer xenografts and correlated these observations with the degree of tumor neovascularization. No direct cytotoxic effects of squalamine against tumor cells were observed in vitro with or without cisplatin. Squalamine was effective in inhibiting the establishment of H460 human tumors in BALBc nude mice but was ineffective in inhibiting the growth of H460, CALU-6, or NL20T-A human tumor xenografts when administered i.p. to mice bearing established tumors. However, when combined with cisplatin or carboplatin, squalamine increased tumor growth delay by > or =1.5-fold in the three human lung carcinoma cell lines compared with cisplatin or carboplatin alone. No enhancement of antitumor activity was observed when squalamine was combined with paclitaxel, vinorelbine, gemcitabine, or docetaxel. Repeated cycles of squalamine plus cisplatin administration delayed H460 tumor growth >8.6-fold. Squalamine plus cisplatin reduced CD31 vessel formation by 25% compared with controls, squalamine alone, or cisplatin alone; however, no inhibition in CD31 vessel formation was observed when squalamine was combined with vinorelbine. These data demonstrate that the combination of squalamine and a platinum analog has significant preclinical antitumor activity against human lung cancer that is related to the anti-angiogenic effects of squalamine.     

In vitro comparative evaluation of trastuzumab (Herceptin) combined with paclitaxel (Taxol) or docetaxel (Taxotere) in HER2-expressing human breast cancer cell lines.

BACKGROUND: Trastuzumab (Herceptin) has clinical indication in association with paclitaxel (Taxol) for the treatment of human epidermal growth factor receptor 2 (HER2)-expressing breast cancer. Synergistic interactions have been reported with taxane derivatives in HER2-expressing breast cancer cells. However, no direct comparison of the potential interest in combining trastuzumab with either paclitaxel or docetaxel (Taxotere) has been reported. MATERIALS AND METHODS: The present study was designed to evaluate in a comparative way the interaction of trastuzumab with paclitaxel or docetaxel in HER2-overexpressing human breast cancer cell lines. HER2 expression was documented in MCF-7, MDA-MB453 and SK-BR3 cell lines using immunocytochemistry with purified mouse anti-human monoclonal antibody. Cytotoxicity assays were performed using the sulforhodamine B assay and in vitro interactions between trastuzumab and taxanes were analyzed using the median-effect principle. RESULTS: Trastuzumab cytotoxicity was confirmed to be directly related to HER2 expression level. At the IC(50), the combination of trastuzumab with either paclitaxel or docetaxel led to synergism in all cell lines. However, considering mean values calculated in the IC(30)-IC(70) range of concentrations, trastuzumab interacted additively with docetaxel in SK-BR3 and MDA-MB453 cell lines while additive and synergistic interactions were achieved with paclitaxel in SK-BR3 and MDA-MB453, respectively. On the same basis, trastuzumab yielded synergistic interaction with both taxanes in the MCF-7 cell line. CONCLUSIONS: The present study shows that at least additive interactions are observed when trastuzumab is combined with either paclitaxel or docetaxel in weak to moderate or more than moderate HER2-expressing cells. Some interesting results were achieved in cells displaying weak HER2 expression which could suggest some further potential interest in trastuzumab.     

Sensitivity of non-small-cell lung cancer cell lines established from patients treated with prolonged infusions of Paclitaxel

OBJECTIVE: Regimens with prolonged infusions of taxanes have been developed for patients with cancer to overcome drug resistance. Our objective of the present study was to examine the impact of prolonged exposure on the cytotoxicity of taxanes against non-small-cell lung carcinoma (NSCLC) cell lines and the clinical response and outcome of the patients. METHODS: Five cell lines (NCI-H2882, -H2887, -H2973, -H3122, -H3255) were derived from previously untreated patients with NSCLC who participated in clinical trials of continuous 96-hour infusions of paclitaxel followed by bolus cisplatin. Two additional cell lines (NCI-H838, -H1299) with previously published data were used as controls. Drug sensitivities were assessed by the MTS (Promega) assay. Multidrug resistance (MDR) phenotypes were assessed by quantitative real-time PCR and HER-2/NEU by both immunohistochemistry and ELISA. RESULTS: The median of mean IC(50) values of docetaxel at the exposure durations of 3, 24, 72 and 120 h were 0.52, 0.06, 0.03 and 0.06 microM, respectively. The median of mean IC(50) values of paclitaxel at the exposure duration of 3, 24, 72 and 120 h were 0.48, 0.13, 0.03 and 0.02 microM, respectively. In all cell lines studied, there was a less than 4-fold difference in the IC(50) values between docetaxel and paclitaxel at 3-, 72-, and 120-hour exposure times. The single cell line with moderate MDR1 expression (NCI-H2887) was the only cell line established from a patient with progressive disease when treated with paclitaxel. CONCLUSIONS: This study demonstrates prolonged exposure to both docetaxel and paclitaxel inhibits the growth of NSCLC cell lines in similar fashion.     

Comparative analysis of xanafide cytotoxicity in breast cancer cell lines

Xanafide, a DNA-intercalating agent and topoisomerase II inhibitor, has previously demonstrated comparable cytotoxicity to the parent drug amonafide (NSC 308847). The current study was conducted to investigate further the anti-proliferative effects of xanafide in human breast cancer cell lines, in vitro and in vivo. The in vitro activity of xanafide against MCF-7, MDA-MB-231, SKBR-3 and T47D cell lines was compared to that of paclitaxel, docetaxel, gemcitabine, vinorelbine and doxorubicin. In MCF-7, xanafide demonstrated comparable total growth inhibition (TGI) concentrations to the taxanes and lower TGI values than gemcitabine, vinorelbine and doxorubicin. MCF-7 (oestrogen receptor (ER)+/p53 wild-type) was the most sensitive cell line to xanafide. MDA-MB-231 and SKBR-3 exhibited similar sensitivity to xanafide. T47 D (ER+/p53 mutated), showed no response to this agent. The in vivo activity of xanafide was further compared to that of docetaxel in MCF-7 and MDA-MB-231 cell lines using the hollow fibre assay. Xanafide was slightly more potent than docetaxel, at its highest dose in MCF-7 cell line, whereas docetaxel was more effective than xanafide in MDA-MB-231 cell line. Our results show that there is no relationship between sensitivity of these cell lines to xanafide and cellular levels of both isoforms of topoisomerase II and suggest that ER and p53 status and their crosstalk may predict the responsiveness or resistance of breast cancer patients to xanafide.     

Docetaxel plus Cisplatin

? Docetaxel and cisplatin are well established antineoplastic agents with activity against NSCLC. The combination exhibited additive cytotoxic activity against human NSCLC cell lines in vitro. ? In a large phase III trial in chemotherapy-naive patients with advanced NSCLC, survival with docetaxel plus cisplatin was statistically noninferior to that with the control regimen of vinorelbine plus cisplatin. Overall response rate with docetaxelplus cisplatin was significantly higher than with the control. ? Median survival times, tumor response rates, and median time to progression for patients receiving docetaxel plus cisplatin were similar to those for patients receiving paclitaxel plus cisplatin in another large phase III trial. ? Neutropenia was the most common grade 3/4 adverse event in docetaxel/cisplatin recipients (≥69% of patients in the two large phase III trials); these proportions were not significantly different from those for patients receiving controls. Grade 3/4 vomiting, nausea, or anemia were significantly less common than with vinorelbine plus cisplatin, whereas hypersensitivity reactions were significantly more common than with paclitaxel plus cisplatin.

Anti-tumor Efficacy of Paclitaxel against Human Lung Cancer Xenografts

We examined paclitaxel for anti-tumor activity against human lung cancer xenografts in nude mice and compared its efficacy with that of cisplatin, currently a key drug for lung cancer chemotherapy. Five non-small cell lung cancers (A549, NCI-H23, NCI-H226, NCI-H460 and NCI-H522) and 2 small cell lung cancers (DMS114 and DMS273) were chosen for this study, since these cell lines have been well characterized as regards in vitro and in vivo drug sensitivity. These cells were exposed to graded concentrations of paclitaxel (0.1 to 1000 nM ) for 48 h. The 50% growth-inhibitory concentrations (GI₅₀) for the cell lines ranged from 4 to 24 n M , which are much lower than the achievable peak plasma concentration of paclitaxel. In the in vivo study, 4 cell lines (A549, NCI-H23, NCI-H460, DMS-273) were grown as subcutaneous tumor xenografts in nude mice. Paclitaxel was given intravenously as consecutive daily injections for 5 days at the doses of 24 and 12 mg/kg/day. Against every xenograft, paclitaxel produced a statistically significant tumor growth inhibition compared to the saline control. Paclitaxel at 24 mg/kg/day was more effective than cisplatin at 3 mg/kg/day with the same dosing schedule as above, although the toxicity of paclitaxel was similar to or rather lower than that of cisplatin, in terms of body weight loss. In addition, paclitaxel showed potent activity against 2 other lung cancer xenografts (NCI-H226 and DMS114). Therefore, paclitaxel showed more effective, wider-spectrum anti-tumor activity than cisplatin in this panel of 6 lung cancer xenografts. These findings support the potential utility of paclitaxel in the treatment of human lung cancer     

Sequence-dependent synergism between the new generation platinum agent ZD0473 and paclitaxel in cisplatin-sensitive and -resistant human ovarian carcinoma cell lines

ZD0473 is a new generation hindered platinum agent currently undergoing worldwide Phase II clinical studies. The in vitro cytotoxicity of ZD0473 either alone or in combination with the anticancer drugs paclitaxel, gemcitabine, vinorelbine, topotecan and doxorubicin was determined using four human ovarian carcinoma cell lines and by the sulphorhodamine B assay (SRB). The lines included one model of acquired cisplatin resistance and one isogenic pair differing only in their p53 status. Notably, the simultaneous exposure to ZD0473 and paclitaxel for 96 h resulted in synergy (as defined by a median effect analysis) in all four cell lines (i.e. independent of cisplatin resistance and p53 status). In addition, synergy was observed in 3/4 lines and 2/4 lines following concomitant exposure to topotecan or gemcitabine, respectively. Sequencing studies with ZD0473 and paclitaxel revealed that, for three of the four cell lines, the combination of ZD0473 administered for 24 h prior to paclitaxel for 24 h conferred a greater growth inhibitory effect than the reverse sequential combination. This scheduling effect was particularly marked for the acquired cisplatin-resistant A2780CisR cell line; synergy being observed with ZD0473/paclitaxel, but antagonism with paclitaxel/ZD0473. This effect did not appear to be correlated with changes in drug-induced cell cycle checkpoints. These data suggest that ZD0473 may be usefully combined with various cytotoxics in the clinic, including paclitaxel, topotecan and gemcitabine.     

Cost-utility analysis of chemotherapy using paclitaxel, docetaxel, or vinorelbine for patients with anthracycline-resistant breast cancer.

PURPOSE: Paclitaxel, docetaxel, and vinorelbine have been approved for chemotherapy in patients with advanced breast cancer that is resistant to anthracyclines. Selecting which agent to use is difficult because each possesses advantages and disadvantages related to clinical response, toxicity, method of administration, and cost. A cost-utility analysis was therefore performed to create a rank order on the basis of effectiveness, quality of life, and economic considerations. PATIENTS AND METHODS: Eighty-eight anthracycline-resistant breast cancer patients who had received paclitaxel (n = 34), docetaxel (n = 29), or vinorelbine (n = 25) during the past 2 years were identified. Total resource consumption was collected, which included expenditures for chemotherapy, supportive care, laboratory tests, management of adverse effects, and all related physician fees. Utilities from 25 oncology care providers and 25 breast cancer patients were estimated using the time trade-off technique. The economic estimates from the chart review and clinical data from the literature were then modeled using the principles of decision analysis. RESULTS: Each of the three drugs led to a similar duration of quality-adjusted progression-free survival (paclitaxel, 37.2 days; docetaxel, 33.6 days; vinorelbine, 38.0 days). Vinorelbine was the least costly strategy, with an overall treatment expenditure of Can $3,259 per patient, compared with Can $6,039 and Can $10,090 for paclitaxel and docetaxel, respectively. CONCLUSION: Palliative chemotherapy with vinorelbine in anthracycline-resistant metastatic breast cancer patients has economic advantages over the taxanes and provides at least equivalent quality-adjusted progression-free survival. These benefits are largely related to its lower drug acquisition cost and better toxicity profile.