恶性肿瘤组织CD8~+/CD28~+细胞表达与细胞凋亡的相关性

目的探讨恶性肿瘤组织中CD8+/CD28+细胞杀伤肿瘤细胞的机制。方法用流式细胞术检测恶性肿瘤组织中CD8+/CD28+细胞表达率及细胞凋亡(APO)水平,并分析两者之间的关系。结果恶性肿瘤组织的CD8+/CD28+细胞检出率为(6.86±4.19)%,显著低于正常对照组织(11.85±3.80)%(P<0.01)。恶性肿瘤组织APO检出率为(1.49±1.24)%,显著低于正常对照组织(4.34±3.28)%,(P<0.01)。在恶性肿瘤组织中,CD8+/CD28+细胞检出率和APO表达水平呈显著正相关(r=0.5995,P<0.01)。结论恶性肿瘤能引起组织中CD8+/CD28+细胞表达率和APO检出率显著下降,且二者检出率呈显著正相关。恶性肿瘤组织中CD8+/CD28+细胞杀伤肿瘤细胞的机制可能与诱导肿瘤细胞凋亡密切相关。     

恶性肿瘤患者手术治疗前后外周血IL-2受体表达(CD+25)细胞的比较

目的　探讨外科手术治疗对恶性肿瘤患者外周血淋巴细胞白细胞介素 -2受体表达水平的影响。方法　用流式细胞术对 70例外科手术前和 43例外科手术后恶性肿瘤患者外周血淋巴细胞白细胞介素 -2受体 (CD+2 5)检出率进行了对比分析。结果　外科手术后恶性肿瘤患者外周细胞CD+2 5细胞检出率显著高于外科手术前患者 (分别为 9 0 3 %± 3 6 2 %和 6 6 6 %± 3 14 % ,P <0 0 1)。结论　外科手术治疗能引起恶性肿瘤患者外周血细胞白细胞介素 -2受体表达率升高。     

放射治疗对恶性肿瘤患者血细胞动力学的影响

目的　探讨放射治疗对恶性肿瘤患者血细胞动力学的影响。方法　用流式细胞术对2 5 7例放射治疗患者和 2 88例未放射治疗患者外周血细胞的增殖活性和细胞凋亡水平进行了对比分析。结果　肿瘤放射治疗患者、未放射治疗患者和正常对照者血细胞S期细胞比率和凋亡水平均有显著差异 ,分别为 1.2 3%± 1.15 %、0 .5 4%± 0 .46 %、0 .33%± 0 .2 6 %和 8.93%± 6 .94%、0 .2 0 %±0 .2 0 %、0 .15 %± 0 .13 % (F =3.18,P <0 .0 5和F =5 .77,P <0 .0 1)。在放射治疗患者中 ,放射治疗后<1个月者的细胞凋亡水平和S期细胞增殖活性均显著高于放射治疗后 1～ 3个月患者 ,分别为16 .5 6 %± 12 .95 %和 1.76 %± 1.75 %、0 .49%± 0 .2 9%和 0 .5 0 %± 0 .48% (t =9.0 6 ,P <0 .0 1和t =4.6 1,P <0 .0 1)。结论　放射治疗能促进恶性肿瘤患者血细胞凋亡水平和增殖活性显著升高。其检出率随时间增加而减低。该结果为探讨肿瘤放射反应提供了新的资料     

抗原致敏树突状细胞诱导CTLs杀伤HL-60细胞作用研究

 目的　探讨树突状细胞 (DC)在体外诱导针对白血病细胞的CTLs杀伤活性。方法　用IL 4和GM CSF培养正常人外周血DC ,以HL 6 0细胞裂解液致敏DC ,再与淋巴细胞共孵育 ,激活T淋巴细胞 ,用LDH释放法测定致敏DC诱导杀伤性细胞对HL 6 0细胞的杀伤活性。结果　外周血单个核细胞经体外扩增培养出可见树突状形状的DC ,流式细胞仪检测细胞表面CD1α及CD86表达阳性 ,CD14表达阴性。混合淋巴细胞反应 (MLR)观察DC刺激的异体淋巴细胞增殖明显较对照组高 ,两者比较有显著性差异 (n =15 ,P <0 .0 1)。在效靶比为 2 0∶1时 ,抗原致敏的DC诱导的杀伤性T细胞对HL 6 0细胞的杀伤率是 39.9%± 2 1.5 % ,直接以抗原刺激的T细胞的杀伤率是 2 6 .3%± 15 .6 %。两组比较差异有非常显著性 (n =16 ,P <0 .0 0 1)。效靶比为 2∶1时 ,抗原致敏的DC诱导的杀伤性T细胞对靶细胞就有明显的杀伤作用 ,随着效靶比增加 ,杀伤作用增强。实验组和对照组不同效靶比杀伤率比较 ,差异有非常显著性 (n =16 ,P <0 .0 0 1)。结论　DC...     

FasL在激活骨髓细胞的表达研究

目的　探讨 Fasl(Fas- L igand)在 ABM(activated bone marrow)杀伤肿瘤细胞效应中的作用。方法　应用抗 CD3 单克隆抗体体外激活骨髓细胞 ,采用免疫荧光标记、流式细胞仪检测 ,观察了不同条件下 ABM细胞表面 Fas L 的表达。结果　未激活的骨髓细胞不表达 Fas L,r IL- 2激活后可见 Fas L 的表达 (7.0 4 %± 3 .4 4% ) ,抗 CD3单抗可促进其表达 (11.84 %± 4 .80 % ) ,三组比较具有显著性差异 (P<0 .0 0 5 )。结论　 ABM杀伤肿瘤细胞的机制与 Fas/ Fas L 介导的肿瘤细胞凋亡有关。     

LMP1通过Survivin抑制60Co诱导鼻咽癌细胞凋亡

目的　研究EB病毒编码的潜伏膜蛋白 1(LMP1)介导凋亡抑制蛋白 (Survivin)表达对辐射效应的影响。方法　利用LMP1可调控表达鼻咽癌细胞系 (Tet on LMP1HNE2 )诱导LMP1表达 ,同时 60 Co照射 5Gy ,采用形态学观察、流式细胞术和半胱氨酸蛋白酶 3(Caspase 3)活性检测等方法 ,分析LMP1表达对60 Co诱导鼻咽癌细胞凋亡的影响。用反义Survivin寡核苷酸阻断Survivin表达 ,观察Sur vivin表达阻断对60 Co辐射效应的影响。结果　LMP1表达抑制60 Co诱导鼻咽癌细胞凋亡 ,LMP1表达60 Co照射组形态学和流式细胞术检测凋亡率 (32 .7%± 2 .1% ,6 .3% )明显低于LMP1表达阴性组 (6 6 .0 %± 3.0 % ,2 9.6 % ) (P <0 .0 5 ) ;转染Survivin反义寡核酸后细胞凋亡率 (5 9.3%± 3.2 % ,3.0 % )明显高于对照组 (2 6 .0 %± 2 .6 % ,8.6 % ) (P <0 .0 5 ) ;同样转染Survivin反义寡核酸组Caspase 3活性 (3.78nmol/ 10 6)高于对照组 (2 .79nmol/ 10 6)。结论　提示LMP1通过介导Survivin表达而抑制60 Co照射诱导凋亡 ,Survivin反义核酸协同辐射诱导肿瘤细胞凋亡 ,Survivin作为增敏放射治疗靶 ,具有潜在的临床意义。     

肿瘤转移相关基因在恶性肿瘤组织中的表达及其临床意义

 目的　探讨各种肿瘤转移相关基因编码蛋白在恶性肿瘤转移中的表达规律及其临床意义。方法　采用流式细胞术对 5 6例肿瘤转移和 6 1例肿瘤未转移患者瘤组织的CD4 4V5 +、CD4 4V6 +、c erbB 2 +、nm2 3+、DCC +和p16 +细胞检出率和DNA含量进行了检测和分析。结果　恶性肿瘤患者瘤组织细胞的CD4 4V5 +、CD4 4V6 +和c erbB 2 +细胞表达率均显著高于正常对照组 (P <0 .0 1或P <0 .0 5 ) ;nm2 3+,DCC +,p16 +细胞表达率则显著低于正常对照组 (P <0 .0 1或P <0 .0 5 )。肿瘤转移者、多器官转移者、DNA异倍体者、SPF增高者、Apo减低者的CD4 4V5 +、CD4 4V6 +、c erbB 2 +细胞表达率均显著高于未转移者、单器官转移者、DNA二倍体者、SPF不增高者、Apo不减低者 (P <0 .0 1或P <0 .0 5 )。而nm2 3+、DCC +、p16 +细胞的表达率与此相反。结论　肿瘤组织肿瘤转移相关基因编码蛋白表达水平的检测 ,对肿瘤的恶性度、转移潜能、转移严重程度及患者预后估计有重要价值。     

加速超分割术前放疗诱导非小细胞肺癌细胞凋亡的研究

目的　探索放射线诱导非小细胞肺癌细胞凋亡及对凋亡相关蛋白Bcl 2、Bax表达的影响。方法　 81例初治的非小细胞肺癌患者 ,分为加速超分割术前放疗组 ( 2 0例 )和单纯手术组 ( 61例 )。术前放疗组采用前后对穿照射 ,2 .5Gy/次 ,2次 /天 ,总量 2 5Gy/10次 /5～ 7天 ,放疗后 2周内手术。用间接免疫荧光法和流式细胞术定量分析细胞凋亡指数 (AI)、细胞周期分布和凋亡相关蛋白Bcl 2和Bax的表达。结果　单纯手术组AI为 4.6%± 2 .3 % ,术前放疗组为 12 .8%± 4.3 % (P <0 .0 0 1)。单纯手术组S期细胞比例 (Sphasefraction ,SPF)为 16.3 %± 4.6% ,术前放疗组为 14 .9%± 4.1% (P >0 .0 5 )。单纯手术组Bcl 2、Bax蛋白免疫荧光指数 (FI)和Bcl 2 /Bax比值分别为 1.3 3± 0 .2 1、1.0 5± 0 .13和 1.2 9± 0 .2 3 ,术前放疗组分别为 1.14±0 .2 6、1.19± 0 .16和 0 .96± 0 .2 3 ,术前放疗组Bcl 2蛋白表达水平下降 (P <0 .0 1) ,Bax蛋白表达水平升高 (P<0 .0 0 1) ,Bcl 2 /Bax比值明显下降 (P <0 .0 0 1)。AI与Bax蛋白表达呈正相关 (P <0 .0 0 1) ,与Bcl 2 /Bax比值呈负相关 (P <0 .0 1)。结论　加速超分割术前放疗使Bcl 2蛋白表达水平下降并诱导Bax蛋白表达水平升高 ,诱发了较高水平的细胞凋亡 ,但是否能提高     

骨肉瘤细胞凋亡与p53基因表达的研究

目的 探讨骨肉瘤细胞凋亡与p53蛋白异常的相关性,p53基因在骨肉瘤细胞凋亡发生中所起作用及两者与骨肉瘤预后的关系.方法 采用末端脱氧核糖核酸转移酶介导的Bio-dUTP末端标记技术(TUNEL)和免疫组化对40例骨肉瘤活检组织的细胞凋亡指数和p53蛋白表达进行检测.结果 骨肉瘤组织中存在细胞凋亡(凋亡/40).p53蛋白阳性组的凋亡%～14%,平均3.1%±3.5%)和p53蛋白异常表达(阳性率为55%、22指数范围为0指数明显低于p53蛋白阴性组(P＜0.01).结论 p53异常可能抑制细胞凋亡.细胞凋亡指数、p53蛋白表达与骨肉瘤病人的预后有关.     

DC与CIK共培养后对白血病细胞杀伤活性的研究

目的研究细胞因子诱导的杀伤细胞(CIK)与同源树突状细胞(DC)共培养后CIK细胞的增殖活性、表型的变化,及其对K562、HL-60白血病细胞细胞毒作用的影响。方法采集健康供者的外周血单个核细胞(MNC),置于37℃,5%CO2培养箱培养2 h,收集非贴壁细胞用于诱导培养CIK细胞,贴壁细胞诱导分化出成熟DC,将成熟DC和CIK细胞按1 5的比例混合培养3天,用MTT法检测DC-CIK共培养细胞杀伤K562和HL-60白血病细胞株的活性。结果DC-CIK共培养后增殖速度明显快于单纯CIK细胞组(P<0.05);培养第14天,CIK中CD3+CD8+、CD3+CD56+双阳性细胞的比率分别为58.6%±7.3和26.5%±6.2,DC-CIK的CD3+CD8+、CD3+CD56+的比率分别为72.5%±4.2和38.4%±6.1,表达差异显著(P<0.05);在2.5∶1~20∶1的效靶比范围内,DC-CIK对K562、HL-60细胞的杀伤活性较单纯CIK细胞组的杀伤活性要高(P<0.05)。结论DC与CIK共培养细胞是增殖活性和细胞毒活性均高于CIK细胞的免疫活性细胞。     

Oxygen for relief of dyspnoea in mildly- or non-hypoxaemic patients with cancer: a systematic review and meta-analysis

The aim of this study was to determine the efficacy of palliative oxygen for relief of dyspnoea in cancer patients. MEDLINE and EMBASE were searched for randomised controlled trials, comparing oxygen and medical air in cancer patients not qualifying for home oxygen therapy. Abstracts were reviewed and studies were selected using Cochrane methodology. The included studies provided oxygen at rest or during a 6-min walk. The primary outcome was dyspnoea. Standardised mean differences (SMDs) were used to combine scores. Five studies were identified; one was excluded from meta-analysis due to data presentation. Individual patient data were obtained from the authors of the three of the four remaining studies (one each from England, Australia, and the United States). A total of 134 patients were included in the meta-analysis. Oxygen failed to improve dyspnoea in mildly- or non-hypoxaemic cancer patients (SMD=-0.09, 95% confidence interval -0.22 to 0.04; P=0.16). Results were stable to a sensitivity analysis, excluding studies requiring the use of imputed quantities. In this small meta-analysis, oxygen did not provide symptomatic benefit for cancer patients with refractory dyspnoea, who would not normally qualify for home oxygen therapy. Further study of the use of oxygen in this population is warranted given its widespread use.     

Endoscopic Endonasal Dacryocystorhinostomy: Best Surgical Management for DCR

EEDCR is a highly rewarding Endoscopic procedure for management of dacryocystitis when epiphora does not respond to medications or repeated syringing of nasolacrimal duct. It is a simple, less time consuming, safe but skilful, highly satisfying surgery both for the patients as well as the surgeons. There is very big advantage of EEDCR, it is close 100% successful procedure, even if there is recurrence of epiphora it is again correctable fully with no residual affects. EEDCR is far more superior to External DCR/Laser DCR and there are definite reasons for it. A total number of 578 cases have been operated by me from April 1, 2005 to March 31, 2011, only very few reoccurrences were there and they were corrected easily so much so that it can be said that it is a close 100% successful procedure and best surgical management of DACRYOCYSTITIS up to date. The successful outcome was defined as symptomatic relief from epiphora and dacryocystitis and a patent nasolacrimal duct upon syringing at the end of procedure and on follow up of patient.     

蛋白激酶C的下调与KBV200细胞多药耐药性的关系

目的　探讨蛋白激酶C (PKC)在肿瘤多药耐药 (MDR)中的作用。方法　3 2 P掺入法测定PKC的活性 ;Westernblot法检测KBV2 0 0细胞株PKC亚型的表达和亚细胞分布 ;实验组用十字孢碱 (SP)预孵育KBV2 0 0细胞 ;MTT法检测耐药株KBV2 0 0细胞的耐药性。结果　SP可下调膜组分和浆组分的PKC活性及总活性 ;使PKCα膜组分和浆组分的表达均降低 ,PKCβ的膜组分消失 ,浆组分PKCβ的表达稍增强 ,PKCε的膜组分和浆组分表达无变化 ;SP可降低VCR、ADR对KBV2 0 0细胞的IC50 值 (P <0 0 1)。结论　SP使KBV2 0 0细胞耐药性降低 ,可能与下调PKC有关。     

洛铂联合多西他赛行肿瘤细胞减灭术加腹腔热灌注化疗治疗腹膜癌的临床观察

目的 分析洛铂联合多西他赛行肿瘤细胞减灭术（cytoreductive surgery, CRS）加腹腔热灌注化疗（hyperthermic intraperitoneal chemotherapy, HIPEC）治疗腹膜癌（peritoneal carcinoma, PC）的围手术期安全性及疗效。 方法 PC患者行CRS+HIPEC治疗,药物为洛铂50 mg/m2、多西他赛60 mg/m²,加入12 000 ml 0.9%氯化钠溶液加热至（43±0.5）℃持续灌注60 min。记录术后6天体温和心率变化、围手术期不良事件、血常规及血生化指标、术后患者恢复情况及生存结果。结果 90例PC患者行95次CRS+HIPEC,手术时间180~450 min (中位数485 min）;术后6天最高体温、心率分别为36.4℃~38.6℃（中位数37.5℃）、76~124 bpm（中位数100 bpm）,严重不良事件16例,包括围手术期死亡2例。中位生存期20.8月（95%CI: 13.1~25.8月）,1、3、5年生存率分别为75.6%、45.6%、43.3%。 结论 洛铂联合多西他赛进行CRS+HIPEC治疗PC安全性可接受,有助于延长患者生存期。     

MNP和MVP方案治疗非小细胞肺癌的临床研究

目的　比较MNP和MVP方案治疗晚期非小细胞肺癌 (NSCLC)的疗效和不良反应。方法　 12 6例晚期NSCLC患者随机分为A和B组 ,A组采用MNP(丝裂霉素 去甲长春花碱 顺铂 )方案化疗。B组采用MVP(丝裂霉素 长春酰胺 顺铂 )方案化疗。至少连用 2个周期后评价疗效。结果　A组有效率为 5 4.0 % ( 3 4/63 ) ,B组有效率为 3 4.9% ( 2 2 /63 ) ,无显著性差异 (P>0 .0 5 ) ;其中对腺癌有效率A组为 44 .4% ( 16/3 6) ,B组为 3 3 .3 % ( 12 /3 6)。A组静脉炎发生率为 2 8.6% ( 14 /4 9) ,B组为 0 (P <0 .0 5 ) ,其它不良反应 2组无显著性差异。结论　MNP方案为治疗晚期NSCLC较为有效和安全的化疗方案     

Bortezomib-related neuropathy may mask CNS relapse in multiple myeloma: A call for diligence

Background: Neuropathy is a common adverse effect of bortezomib. Isolated central nervous system (CNS) relapse in MM remains exceedingly rare and carries a dismal prognosis. We present an unusual case of bortezomib related neuropathy masking a CNS relapse of MM. Case presentation: A 57-year-old female was diagnosed with standard-risk MM with clinical and cytogenetic features not typically associated with CNS involvement. She was treated with 4 cycles of bortezomib/cyclophosphamide/dexamethasone (VCD) and achieved a VGPR, after which she underwent an autologous stem cell transplant (ASCT) followed by bortezomib maintenance. Six months after ASCT she developed symptoms suggestive of peripheral neuropathy which was attributed to bortezomib. However the symptoms persisted despite discontinuation of bortezomib. Imaging and cerebrospinal fluid analysis subsequently confirmed a CNS relapse. Discussion: CNS involvement in MM (CNS-MM) is uncommon and is considered an aggressive disease. Recently published literature has reported biomarkers with prognostic potential. However, isolated CNS relapse is even less common; an event which carries a very poor prognosis. Given the heterogeneous neurologic manifestations associated with MM, clinical suspicion may be masked by confounding factors such as bortezomib-based therapy. The disease may further remain incognito if the patient does not exhibit any of the high risk features and biomarkers associated with CNS involvement. Conclusion: In the era of proteasome inhibitor (PtdIns)/immunomodulator (IMID)-based therapy for MM which carries neurologic adverse effects, it is prudent to consider CNS relapse early. This case further highlights the need for more robust biomarkers to predict CNS relapse and use of newer novel agents which demonstrate potential for CNS penetration.     

HIA与IA方案治疗初治急性髓系白血病的临床对比观察

目的分别用去甲氧柔红霉素（IDA）与HA方案[高三尖杉酯碱（HH）+阿糖胞苷（Ara-C）]组成的双诱导HIA方案与传统IA方案治疗初治急性髓系白血病,比较两组化疗方案的疗效及不良反应。方法HIA方案为：IDA 7 mg/（m²·d）,静脉滴注第1~3天;HH 2.5 mg/（m²·d）,静脉滴注,第1~5天;Ara-C 100 mg/（m²·d）,静脉滴注,第1~5天。IA方案为：IDA 10 mg/（m²·d）,静脉滴注,第1~3天; Ara-C 100 mg/（m²·d）,静脉滴注,第1~5天。结果HIA方案组第一疗程 74.4%（32/43）获CR,其中9例复发（早期复发1例,晚期复发8例）。IA方案组第一疗程73.3%(26/30）达CR,其中8例复发（早期复发5例,晚期复发3例）。两组在CR率和生存分析比较上差异均无明显统计学意义。但HIA方案组患者心脏不良反应发生率（2.3%）显著低于IA组（16.7%）。HIA方案化疗的不良反应主要为骨髓抑制和粒细胞缺乏所致感染,未见严重的非造血系统不良反应,尤其未加重心脏毒性,治疗过程中未发生早期死亡。结论HIA方案可以减少蒽环类药物的剂量,不加重心脏毒性,增加了患者的耐受能力,且不影响疗效。     

The prognostic role of lymphovascular invasion and lymph node metastasis in perihilar and intrahepatic cholangiocarcinoma

IntroductionCholangiocellular carcinoma (CCA) is an aggressive malignancy with a dismal prognosis. Among curative treatment options for CCA, radical surgical resection with extrahepatic bile duct resection, hepatectomy and en-bloc lymphadenectomy are considered the mainstay of curative therapy. Here, we aimed to identify prognostic markers of clinical outcome in CCA-patients who underwent surgical resection in curative intent.Material and methodsBetween 2011 and 2016, 162 patients with CCA (perihilar CCA (pCCA): n = 91, intrahepatic CCA (iCCA): n = 71) underwent surgery in curative intent at our institution. Preoperative characteristics, perioperative data and oncological follow-up were obtained from a prospectively managed institutional database. The associations of overall- (OS) and disease-free-survival (DFS) with clinico-pathological characteristics were assessed using univariate and multivariable cox regression analyses.ResultsThe median OS and DFS were 38 and 36 months for pCCA and 25 and 13 months for iCCA, respectively. Lymphovascular invasion (LVI) and lymph node metastasis as well as surgical complications as assessed by the comprehensive complication index (CCI) and tumor grading were independently associated with OS for the pCCA (LVI; RR = 2.36, p = 0.028; CCI; RR = 1.04, p < 0.001) and iCCA cohorts (N-category; RR = 3.21, p = 0.040; tumor grading; RR = 3.75, p = 0.013; CCI, RR = 4.49, p = 0.010), respectively. No other clinical variable including R0-status and Bismuth classification was associated with OS.ConclusionMajor liver resections for CCA are feasible and safe in experienced high-volume centers. Lymph node metastasis and LVI are associated with adverse clinical outcome, supporting the role of systematic lymphadenectomy. The assessment of LVI may be useful in identifying high-risk patients for adjuvant treatment strategies.     

Suppression of NAD(P)H-quinone oxidoreductase 1 enhanced the susceptibility of cholangiocarcinoma cells to chemotherapeutic agents

Background

Cholangiocarcinoma (CCA) is highly resistant to most of the known chemotherapeutic treatments. NAD(P)H-quinone oxidoreductase 1 (NQO1) is an antioxidant/detoxifying enzyme recently recognized as an important contributor to chemoresistance in some human cancers. However, the contribution of NQO1 to chemotherapy resistance in CCA is unknown.

Methods

Two CCA cell lines, KKU-100 and KKU-M214, with high and low NQO1 expression levels, respectively, were used to evaluate the sensitivity to chemotherapeutic agents; 5-fluorouracil (5-FU), doxorubicin (Doxo), and gemcitabine (Gem). NQO1 and/or p53 expression in KKU-100 cells were knocked down by siRNA. NQO1 was over-expressed in KKU-M214 cells by transfection with pCMV6-XL5-NQO1 expression vector. CCA cells with modulated NQO1 and/or p53 expression were treated with chemotherapeutic agents, and the cytotoxicity was assessed by SRB assay. The mechanism of enhanced chemosensitivity was evaluated by Western blot analysis.

Results

When NQO1 was knocked down, KKU-100 cells became more susceptible to all chemotherapeutic agents. Conversely, with over-expression of NQO1 made KKU-M214 cells more resistant to chemotherapeutic agents. Western blot analysis suggested that enhanced chemosensitivity was probably due to the activation of p53-mediated cell death. Enhanced susceptibility to chemotherapeutic agents by NQO1 silencing was abolished by knockdown of p53.

Conclusions

These results suggest that inhibition of NQO1 could enhance the susceptibility of CCA to an array of chemotherapeutic agents.     

HMVP与MVP方案治疗晚期非小细胞肺癌的临床研究

目的 :旨在观察羟基喜树碱 (hydroxycamptothecin ,HCPT)联合丝裂霉素 (mitomycin ,MMC)、长春花碱酰胺 (vindesine ,VDS)和顺铂 (cisplatin ,DDP)组成的HMVP和MVP方案治疗晚期NSCLC的近期、远期疗效和毒副反应。方法 :将 90例晚期NSCLC患者随机分为HMVP组 (4 6例 )与MVP组 (4 4例 ) ,观察两组的近期及远期疗效、毒副反应和生存情况。结果 :HMVP和MVP有效率分别为 39.5 4 %和 35 .5 7% ,两组之间无显著性差异 (P >0 .0 5 ) ;两组的中位缓解期、中位生存期、一年及二年生存率亦无明显差异。两组的Ⅲ～Ⅳ度白细胞抑制率、Ⅲ～Ⅳ度血小板抑制率、Ⅲ～Ⅳ度恶心 /呕吐发生率、Ⅲ～Ⅳ度便秘发生率之间均无显著性差异 (P >0 .0 5 )。结论 :MVP方案治疗晚期NSCLC的疗效略低于HMVP方案 ,但后者未显示出明显的疗效优势 ,却可能增加白细胞抑制、恶心 /呕吐和便秘的发生率 ,也增加了患者的经济负担 ;故在NSCLC化疗中宜选择MVP方案