Solamargine induces apoptosis and sensitizes breast cancer cells to cisplatin.

Solamargine (SM), a major steroidal alkaloid glycoside, was purified from Solanum incanum plant. SM exhibited the most cytotoxic effect comparing with that of cisplatin (cDDP), methotrexate (MTX), 5-fluorouracil (5-FU), epirubicin (EPI) and cyclophosphamide (CP) against human breast cancer cells. In this study, SM induces apoptosis of the breast cancer cells and the mechanism was characterized. SM up-regulated the expressions of external death receptors, such as tumor necrosis factor receptor I (TNFR-I), Fas receptor (Fas), TNFR-I-associated death domain (TRADD), and Fas-associated death domain (FADD). SM also enhanced the intrinsic ratio of Bax to Bcl-2 by up-regulating Bax and down-regulating Bcl-2 and Bcl-xL expressions. These effects resulted in the release of mitochondrial cytochrome c and activation of caspase-8, -9 and -3 in the cells, indicating that SM triggered extrinsic and intrinsic apoptotic pathways of breast cancer cells. Similar to function way of SM, cDDP causes cancer cell apoptosis though caspase-8/caspase-3 and Bax/cytochrome c pathways, but the resistance to cDDP is correlated with Bcl-2 and Bcl-xL overexpression. However, the overexpression of Bcl-2 and Bcl-xL can be broken through by SM. The combined treatment of SM and cDDP significantly reduced Bcl-2 and Bcl-xL expressions, and enhanced Bax, cytochrome c, caspase-9 and -3 expressions in breast cancer cells. Thus, the combined use of SM and cDDP may be effective in cDDP-resistant breast cancer.     

卡培他滨联合顺铂治疗晚期乳腺癌的临床研究

目的 探讨卡培他滨联合顺铂治疗蒽环类及紫杉类耐药的晚期乳腺癌的临床效果.方法 选取解放军第三二三医院肿瘤中心的19例蒽环类及紫杉类耐药的晚期乳腺癌患者,给予卡培他滨联合顺铂治疗,21 d为1个周期,所有患者均治疗2个周期以上,观察临床疗效及不良反应.结果 19例患者中完全缓解1例,部分缓解9例,稳定6例,进展3例,总有效率为52.6％.中位无疾病进展生存期6.0个月（95％CI：4.4 ～7.6个月）,中位生存期15.0个月（95％ CI：13.0 ～ 16.9个月）.主要的毒性反应有骨髓抑制、乏力、胃肠道反应及手足综合征等,为可逆性,无治疗相关死亡.结论 卡培他滨联合顺铂疗效较好,毒性反应可耐受,可作为蒽环类及紫杉类耐药的晚期乳腺癌患者的治疗选择.     

多西紫杉醇联合顺铂治疗蒽环类耐药的晚期乳腺癌的临床疗效观察

目的观察多西紫杉醇联合顺铂治疗蒽环类耐药的晚期乳腺癌的疗效与不良反应。方法 2003年6月至2007年6月,我科以多西紫杉醇联合顺铂治疗蒽环类耐药的晚期乳腺癌36例。多西紫杉醇75mg/m2,静脉点滴,第1天;顺铂30mg/（m2.d）,静脉点滴,第1天至第3天;每21d为一周期,至少两个周期后评价疗效。本组中位化疗周期数为4（2-6）周期。结果 36例均可评价疗效。完全缓解（CR）2例（5.6%）,部分缓解（PR）18例（50%）,稳定（SD）9例（25%）,进展（PD）7例（19.4%）,总有效率（CR＋PR）55.6%,中位肿瘤进展时间6个月,一年生存率71%,中为生存时间16个月。主要的不良反应为胃肠道反应和骨髓抑制。结论多西紫杉醇联合顺铂治疗蒽环类耐药的晚期乳腺癌疗效较好,不良反应可以耐受,是蒽环类耐药的晚期乳腺癌的有效解救方案。     

氨磷汀联合吉西他滨与顺铂方案治疗晚期乳腺癌的临床研究

目的观察分析氨磷汀联合吉西他滨与顺铂治疗晚期乳腺癌的疗效和安全性。方法选取我院经病理确诊的52例晚期乳腺癌患者,随机分为试验组及对照组。试验组29例,应用氨磷汀500 mg/m~2,化疗开始前30 min静脉滴注;吉西他滨1 000 mg/m~2静点,第1、8天;顺铂30 mg/m~2避光静点,第1~3天。对照组23例,应用吉西他滨联合顺铂,剂量及用法同试验组。两组均以3周为1个周期。结果 52例均纳入分析,试验组、对照组的有效率分别为37.9%、47.8%,疾病控制率为70.3%、78.2%,两组比较差异无统计学意义(P>0.05)。与对照组比较,试验组骨髓抑制及周围神经毒性发生率明显降低,头晕的发生率升高,而两组肝肾功能损伤、恶心呕吐等例数比较差异无统计学意义。结论氨磷汀联合吉西他滨与顺铂治疗晚期乳腺癌,可减轻骨髓抑制及周围神经毒性,对治疗效果无影响。     

NVB联合顺铂治疗蒽环类化疗后的晚期乳腺癌30例疗效分析

目的 观察NVB联合顺铂治疗蒽环类化疗后晚期乳腺癌的临床疗效.方法 将我院2010年9月至2011年8月我院收治的60例蒽环类化疗后晚期乳腺癌患者按照随机数表分为试验组和对照组各30例,试验组应用NVB联合顺铂治疗,对照组持续使用蒽环类化疗,观察疗效.结果 试验组治疗有效率为43.3％,高于对照组的13.3％,差异有显著性(P＜0.05).经3个疗程后,所有患者均无严重肝功能损伤,主要用药毒副作用为骨髓抑制、胃肠道反应和脱发,少数患者表现为外周神经毒性和静脉炎,在骨髓抑制方面试验组优于对照组(P＜0.05).结论 NVB是蒽环类化疗后晚期乳腺癌患者的首选治疗方案,值得推广应用.     

24例乳腺癌患者术后结合放射治疗的临床观察

目的观察乳腺癌术后放射治疗的疗效。方法24例术后接受乳腺切线照1/4线束6 MV X线50 Gy,局部加量9～12 Mev电子线15 Gy,锁骨上区1/2线束6MV X线50 Gy,腋顶区补量6 MV X线10 Gy的放射治疗。结果在随访1年中的24例中有1例死于肿瘤转移,全组出现复发与转移共3例。并仅1例放疗后乳头脱落,其余病例治疗后前及键侧乳房相比均无明显差别。结论乳腺癌术后放疗可降低局部复发率,同时加强护理,可以提高治疗效果。     

Redox-sensitive,PEG-shielded carboxymethyl PEI nanogels silencing MicroRNA-21, sensitizes resistant ovarian cancer cells to cisplatin

A series of branched polyethylenimine(PEI) modifications including PEGylation(PEG2 k-PEI) for steric shielding, redox-sensitive crosslinking for synthesis PEG2 k-PEI-ss nanogels and subsequent carboxymethylation(PEG2 k-CMPEI-ss) for modulation of the polymer pk a have been introduced for cellular delivery of Anti-mi R-21. The synthesis was characterized using 1 H NMR, FTIR, TNBS, potentiometric titration, particle size and ζ potential. Loading of Anti-mi R-21 at various N/P ratios was investigated by gel retardation, ethidium bromide dye exclusion, heparin sulfate competition and DNase I digestion experiments. The mi R-21 silencing was measured by stem-loop RT PCR in A2780 ovarian cancer cell lines whether it is sensitive to resistant to cisplatin. It has been shown that PEG2 k-CMPEI-ss was well suited for delivery of Anti-mi R-21 in terms of nucleic acid loading, preservation against extracellular matrix and nucleases and sequence-specific silencing of mi RNA-21 in vitro. Moreover, it has been demonstrated that pre-treating cells with Anti-mi R-21 loaded nanogels can sensitize them to cis-Pt even at non-toxic concentraions. The results indicate that PEG2 k-CMPEIss mediated micro RNA delivery can be considered as a novel strategy for ovarian cancer therapy.     

Caveolae/caveolin-1 are important modulators of store-operated calcium entry in Hs578/T breast cancer cells

Caveolin-1 is a principal component of caveolae, invaginations of the plasma membrane that are enriched in cholesterol and sphingolipids. The expression of caveolin-1 has been shown to be tightly correlated to the progression of breast cancer tumors. However, the consequences of altered caveolin-1 expression during tumor progression still remain unclear. Modification of caveolin-1 expression modulates store-operated Ca(2+) entry (SOCE) in various cell types. SOCE is a ubiquitous Ca(2+) entry pathway that previous studies have linked to apoptosis and tumor progression in prostate cancer cells. In this study, we tested the effect of altering caveolin-1 expression on SOCE in Hs578/T breast cancer cells. Through overexpression of caveolin-1 and small hairpin RNA (shRNA) knockdown, we generated four stable cell lines that have 3 different caveolin-1 protein levels. Cav-1 overexpression could increase SOCE activity, while knockdown of caveolin-1 significantly reduced SOCE activity. These functional consequences were correlated with changes in caveolae number in Hs578/T cells. Our results suggest alteration of SOCE by caveolin-1 expression changes could be one of the mechanisms contributing to the progression of breast cancer.     

Silibinin sensitizes chemo-resistant breast cancer cells to chemotherapy

Context: Multiple drug resistance is the major obstacle to conventional chemotherapy. Silibinin, a nontoxic naturally occurring compound, has anticancer activity and can increase the cytotoxic effects of chemotherapy in various cancer models.

Objective: To evaluate the effects of silibinin on enhancing the sensitivity of chemo-resistant human breast cell lines to doxorubicin (DOX) and paclitaxel (PAC).

Materials and methods: The cells were treated with silibinin (at 50 to 600?μM concentrations) and/or chemo drugs for 24 and 48?h, then cell viability and changes in oncogenic proteins were determined by MTT assay and Western blotting/RT-PCR, respectively. Flow cytometry was used to study apoptosis in the cells receiving different treatments. The antitumorigenic effects of silibinin (at 200 to 400?μM concentration) were evaluated by mammosphere assay.

Results: Silibinin exerted significant growth inhibitory effects with IC₅₀ ranging from 200 to 570?μM in different cell lines. Treatment of DOX-resistant MDA-MB-435 cells with silibinin at 200?μM reduced DOX IC₅₀ from 71 to 10?μg/mL and significantly suppressed the key oncogenic pathways including STAT3, AKT, and ERK in these cells. Interestingly treatment of DOX-resistant MDA-MB-435 cells with silibinin at 400?μM concentration for 48?h induced a 50% decrease in the numbers of colonies as compared with DMSO-treated cells. Treatment of PAC-resistant MCF-7 cells with silibinin at 400?μM concentration generated synergistic effects when it was used in combination with PAC at 250?nM concentration (CI?=?0.81).

Conclusion: Silibinin sensitizes chemo-resistant cells to chemotherapeutic agents and can be useful in treating breast cancers.     

Nanomedicines modulating tumor immunosuppressive cells to enhance cancer immunotherapy

Cancer immunotherapy has veered the paradigm of cancer treatment. Despite recent advances in immunotherapy for improved antitumor efficacy, the complicated tumor microenvironment (TME) is highly immunosuppressive, yielding both astounding and unsatisfactory clinical successes. In this regard, clinical outcomes of currently available immunotherapy are confined to the varied immune systems owing in large part to the lack of understanding of the complexity and diversity of the immune context of the TME. Various advanced designs of nanomedicines could still not fully surmount the delivery barriers of the TME. The immunosuppressive TME may even dampen the efficacy of antitumor immunity. Recently, some nanotechnology-related strategies have been inaugurated to modulate the immunosuppressive cells within the tumor immune microenvironment (TIME) for robust immunotherapeutic responses. In this review, we will highlight the current understanding of the immunosuppressive TIME and identify disparate subclasses of TIME that possess an impact on immunotherapy, especially those unique classes associated with the immunosuppressive effect. The immunoregulatory cell types inside the immunosuppressive TIME will be delineated along with the existing and potential approaches for immunosuppressive cell modulation. After introducing the various strategies, we will ultimately outline both the novel therapeutic targets and the potential issues that affect the efficacy of TIME-based nanomedicines.     

Pharmacological profile of store-operated Ca(2+) entry in intrapulmonary artery smooth muscle cells

Store-operated Ca(2+) entry (SOCE) plays an important role in the contraction and proliferation of pulmonary artery smooth muscle cells (PASMCs). The aim of this study was to characterise the pharmacological properties of the SOCE pathway in freshly isolated PASMCs from rat lung and to determine whether this Ca(2+) entry pathway is sensitive to nitric oxide donor drugs. Following depletion of Ca(2+) from the sarcoplasmic reticulum, by treating cells with thapsigargin, re-addition of Ca(2+) produced an increase in cytosolic fluo-4 fluorescence that was sustained for the period that extracellular Ca(2+) was present. Thapsigargin also increased the rate of quench of fura-2 fluorescence, confirming that SOCE was activated. The SOCE pathway was not affected by nifedipine or verapamil; however, it was inhibited by the divalent cations Ni(2+) (10 microM) and Cd(2+) (10 microM) by 47+/-5% and 49+/-5% respectively. SOCE was also inhibited 42+/-5% by 2-aminoethoxydiphenyl borate (2-APB; 75 microM) and 58+/-4% by Gd(3+) (10 microM), although La(3+) (100 microM) had little effect. None of the NO donors examined, including sodium nitroprusside, glyceryl trinitrate, and 2-(N,N-diethylamino)-diazenolate-2-oxide had any effect on SOCE. Thus, the pulmonary vasorelaxation produced by NO does not involve direct inhibition of SOCE in PASMCs. Western blot and immunocytochemistry using antibodies directed against specific TRPC subunits detected the presence of TRPC1, 3, and 6 in pulmonary artery and the pharmacological profile of SOCE in PASMCs favours a role for TRPC1 in mediating the underlying channels that are activated by store depletion.     

STI571 sensitizes breast cancer cells to 5-fluorouracil, cisplatin and camptothecin in a cell type-specific manner

Previously, we demonstrated that Abl kinases are highly active in invasive breast cancer cell lines, and contribute to survival in response to nutrient deprivation, invasion and proliferation. To determine whether an Abl kinase inhibitor, STI571 (Gleevec; imatinib mesylate) sensitizes breast cancer cells to chemotherapeutic agents, we treated three breast cancer cell lines (BT-549, MDA-MB-231, and MDA-MB-468) that have active Abl kinases, with STI571 in combination with several conventional chemotherapeutic drugs frequently used to treat breast cancer, and assessed the effect on cell viability, proliferation, and apoptosis. We found that STI571 had synergistic effects with cisplatin in BT-549 and to some extent in MDA-MB-468 cells; synergized with camptothecin using an alternate dosing regimen in MDA-MB-231 cells; and STI571 synergistically sensitized MDA-MB-468 cells to paclitaxel and to high doses of 5-fluorouracil. Significantly, STI571 increased the ability of cisplatin to inhibit constitutive activation of PI3K/Akt in BT-549 cells, synergized with camptothecin to increase the stability of IκB in MDA-MB-231 cells, and in MDA-MB-468 cells, camptothecin and 5-fluorouracil inhibited STI571-dependent activation of STAT3. In other cell line/drug combinations, STI571 had additive or antagonistic effects, indicating that the ability of STI571 to sensitize breast cancer cells to chemotherapeutic agents is cell type-dependent. Significantly, unlike cisplatin, paclitaxel, and camptothecin, mechloroethamine was strongly antagonistic to STI571, and the effect was not cell line-dependent. Taken together, these data indicate that the cellular milieu governs the response of breast cancer cells to STI571/chemotherapeutic combination regimens, which suggests that treatment with these combinations requires individualization.     

Bone-seeking nanoplatform co-delivering cisplatin and zoledronate for synergistic therapy of breast cancer bone metastasis and bone resorption

The “vicious cycle” established between tumor growth and osteolysis aggravates the process of breast cancer bone metastasis, leading to life-threatening skeletal-related events that severely reduce survival and quality of life. To effectively interrupt the “vicious cycle”, innovative therapeutic strategies that not only reduce osteolysis but also relieve tumor burden are urgently needed. Herein, a bone-seeking moiety, alendronate (ALN), functionalized coordination polymer nanoparticles (DZ@ALN) co-delivering cisplatin prodrug (DSP) and antiresorptive agent zoledronate (ZOL) via Zn²⁺ crosslinking for combination therapy was reported. The versatile DZ@ALN with a diameter of about 40 nm can cross the fissure in the bone marrow sinus capillaries, and possesses an excellent bone-seeking ability both in vitro and in vivo. Additionally, DZ@ALN could synergistically inhibit the proliferation of cancer cells, suppress the formation of osteoclast-like cells and induce the apoptosis of osteoclasts in vitro. Importantly, it could preferentially accumulate in bone affected site, remarkably inhibit the proliferation of tumor cells, relieving bone pain, and significantly inhibit the activation of osteoclasts, protecting the bone from destruction in vivo, eventually leading to the breakdown of “vicious cycle” without inducing obvious systemic toxicity. This innovative nanoagent combines chemotherapy and osteolysis inhibition, exhibiting an inspiring strategy for effective treatment of bone metastasis.     

多西他赛和吉西他滨分别联合顺铂治疗晚期非小细胞肺癌效果比较

目的 比较多西他赛与吉西他滨联合顺铂方案治疗晚期非小细胞肺癌(NSCLC)的临床疗效及不良反应.方法 120例晚期非小细胞肺癌患者完全随机分为2组.多西他赛组60例给予多西他赛37.5 mg/m2,第1、8天;顺铂25 mg/m2,第1～3天.吉西他滨组60例给予吉西他滨1000 mg/m2,第1、8天;顾铂用量同前.化疗每3周重复,每周期评价不良反应,评价疗效并随访生存期.结果 20例患者均可评价疗效和不良反应,2组有效率分别为多西他赛组45.0%(27/60)和吉西他滨组43.3%(26/60),1年生存率分别为45%和43.3%,两组之间有效率和1年生存率均无统计学意义(P＞0.05).不良反应主要为骨髓抑制和肝功能损害[多西他赛组白细胞产减少率为85.0%(51/60),吉西他滨组为78.0%(47/60),2组差异无统计学意义(P＞0.05);2组肝功能损害率分别为33.3%(20/60)、26.7%(16/60),差异有统计学意义(P＜0.05)].结论 多西他赛与吉西他滨联合顺铂方案治疗晚期NSCLC均具有较好的疗效,且两者的疗效相似,不良反应可以耐受,可以作为临床一线治疗.

Abstract：

Objective To compare the efficacy and safety of docetaxel plus cisplatin and gemcitabine plus cisplatin in advanced non-small cell lung cancer (NSCLC). Methods A total of 120 patients with advanced NSCLC were divided into two groups. The patients received docetaxel in docetaxel group. In gemcitabine group the patients received gemcitabine and cisplatin. The treatment schedule was repeated every 3 weeks. The toxicity,quality response and survival rate of life were evaluated after every cycle. Results The response rates of the docetaxel group and the gemcitabine group were 45% and 43.3%,respectively. One-year survival rates in the two groups were 45% and 43.3%,respectively. The response rate,one-year survival time showed no significance (P ＞0.05). The main side effects were myelosupp ression,nausea and vomiting. Conclusion Regimens of DC and GC are both safe and effective in the treatment of advanced stage NSCLC. They can be used as the first regimen of chemotherapy in patients with advanced stage NSCLC.     

RIP3 overexpression sensitizes human breast cancer cells to parthenolide in vitro via intracellular ROS accumulation

Aim： Receptor-interacting protein 3 （RIP3） is involved in tumor necrosis factor receptor signaling, and results in NF-KB-mediated prosurvival signaling and programmed cell death. The aim of this study was to determine whether overexpression of the RIP3 gene could sensitize human breast cancer cells to parthenolide in vitro. Methods： The expression of RIP3 mRNA in human breast cancer cell lines （MCF-7, MDA-MB-231, MDA-MB-435 and T47D） was detected using RT-PCR. Both MDA-MB-231 and MCF-7 cells were transfected with RIP3 expression or blank vectors via lentivirus. Cell viability was measured with MTT assay; intracellular ROS level and cell apoptosis were analyzed using flow cytometry. Results： RIP3 mRNA expression was not detected in the four human breast cancer cell lines tested. However, the transfection induced higher levels of RIP3 protein in MCF-7 and MDA-MB-231 cells. Furthermore, overexpression of RIP3 decreased the IC50 values of parthenolide from 17.6 to 12.6 μmol/L in MCF-7 cells, and from 16.6 to 9.9 μmol/L in MDA-MB-231 cells. Moreover, overexpression of RIP3 significantly increased parthenolide-induced apoptosis and ROS accumulation in MCF-7 and MDA-MB-231 cells. Pretreatment with N-acetyl-cysteine abrogated the increased sensitivity of RIP3-transfected MCF-7 and MDA-MB-231 cells to parthenolide. Conclusion： Overexpression of RIP3 sensitizes MCF-7 and MDA-MB-231 breast cancer cells to parthenolide in vitro via intracellular ROS accumulation.     

Blockade of calcium entry in smooth muscle cells by the antidepressant imipramine

The present study was designed to evaluate the effects of antidepressants on smooth muscle contractile activity. In rat aortic rings, the antidepressants imipramine, mianserin and sertraline provoked concentration-dependent inhibitions of the mechanical responses evoked by K+ (30 mM) depolarization. These myorelaxant effects were not modified by the presence of glibenclamide or 80 mM K+ in the bathing medium. Moreover, the vasodilator properties of imipramine were not affected by atropine, phentolamine and pyrilamine. Radioisotopic experiments indicated that imipramine failed to enhance 86Rb outflow from prelabelled and perifused aortic rings whilst counteracting the increase in 45Ca outflow provoked by a rise in the extracellular K+ concentration. Simultaneous measurements of contractile activity and fura-2 fluorescence revealed that, in aortic rings, imipramine reduced the mechanical and fluorimetric response to K+ challenge. In A7r5 smooth muscle cells, whole cell recordings further demonstrated that imipramine inhibited the inward Ca2+ current. Under different experimental conditions, the ionic and relaxation responses to the antidepressants were reminiscent of those mediated by the Ca2+ entry blocker verapamil. Lastly, it should be pointed out that imipramine exhibited a myorelaxant effect of similar amplitude on rat aorta and on rat distal colon. All together, these findings suggest that the myorelaxant properties of imipramine, and probably also setraline and mianserin, could result from their capacity to inhibit the voltage-sensitive Ca2+ channels.     

超声造影对乳腺纤维腺瘤和乳腺癌的诊断价值

目的研究乳腺纤维腺瘤和乳腺癌的超声造影表现,初步探讨超声造影在乳腺良恶性肿瘤鉴别诊断中的应用价值。方法回顾性分析18例乳腺纤维腺瘤和12例乳腺癌的超声造影表现,对比造影前后肿块的超声表现。结果造影后,14例乳腺纤维腺瘤大小测值无明显变化,4例测值增大,5例乳腺癌大小测值无明显变化,7例乳腺癌者大小测值增大;造影后,纤维腺瘤肿块内血管数大部分无明显变化,血管形态较狭窄平直,沿肿块周边走行,乳腺癌肿块内血管数明显增多增粗、迂曲,并有血管进入肿块内。结论超声造影对显示肿块实际大小优于普通超声,造影后肿块大小测值变大、血管数增多、血管不规则走行等以乳腺癌多见。超声造影有利于提高乳腺癌的正确诊断率。     

Embryonic signature in breast cancers; Pluripotency roots of cancer stem cells

Drug discovery programs for preclinical oncology typically select compounds which have a predilection for inducing cytotoxic effects in cancer cell lines and subsequently, for inhibiting the growth of the transplanted cancer cells in vivo (Winquist et al., 2010). Unfortunately, the cytotoxic effect in vitro and inhibition of tumor growth in animal models are not the end story for curing cancer in preclinical models. The reason behind that is the exciting of small sub type of cells that are relatively resistance to therapy and able to repopulate in vivo, called cancer stem cells (CSCs). O leis et al. recently reported that the pluripotency gene Sox2 but not Oct4 or Nanog is expressed in early stage of breast tumor. Furthermore, the authors demonstrated that Sox2 downregulation, inhibited mammosphere formation and delayed tumor formation in xenograft tumor initiation models (Leis et al., 2012). In this review, we will shed the light on the importance of Sox2 in breast and other tissue tumorigenesis and associated aggressiveness.     

不同化疗方案治疗乳腺癌临床效果比较

目的 探讨不同治疗方案对乳腺癌患者的临床效果.方法 回顾性分析24侧乳腺癌患者的临床资料.根据治疗方法不同分为两组,长春瑞滨联合顺铂治疗(长春瑞滨组)12例,吉西他滨联合顺铂治疗(吉西他滨组)12例,两组均治疗6周,随访1～2个月,观察两组患者治疗后的近期疗效和毒副反应变化.结果 治疗6周后患者总有效率(完全缓解+部分缓解)均优于治疗1周后,差异有统计学意义(P＜0.05);两组间相比,治疗后吉西他滨组患者的总有效率优于长春瑞滨组,但差异无统计学意义(P＞0.05).两组间相比,长春瑞滨组白细胞减少、恶心呕吐及静脉炎的发生率相对较吉西他滨组高,吉西他滨组血小板减少高于长春瑞滨组,差异均有统计学意义(均P＜0.05).结论 吉西他滨联合顺铂治疗乳腺癌疗效显著.     

多西他赛联合顺铂治疗晚期乳腺癌30例

目的观察多西他赛联合顺铂方案治疗晚期乳腺癌患者的临床疗效及引起的不良反应。方法对郑州市消防支队卫生队收治的30例经病理组织学确诊的晚期乳腺癌患者进行多西他赛35mg/m2,静脉滴注1h,第1、8、15d,化疗前1d给予地塞米松每次7.5mg,每日2次,连用3d。顺铂20mg/m2,静脉滴注第1～5d。21d为1个周期,至少应用2个周期后按照WHO标准进行疗效评价。结果晚期乳腺癌30例中完全缓解(CR)4例,部分缓解(PR)15例,稳定(SD)7例,进展(PD)4例,总有效率(PR+CR)为63%,无严重不良反应。结论多西他赛联合顺铂治疗晚期乳腺癌疗效确切,不良反应可以耐受,临床可广泛推广。