奥沙利铂与5-FU联合治疗晚期消化道癌疗效分析

目的 观察奥沙利铂与5-FU方案治疗消化道晚期肿瘤。方法 奥沙利铂150mg／m^2静滴第1天，5-FU300／m^2静滴第1～5天。结果 总有效率胃癌63％，大肠癌67％。结论 此方案治疗消化道肿瘤疗效肯定，毒副反应轻。     

免疫受损大鼠感染铜绿假单胞菌时细胞间黏附分子1及基质金属蛋白酶2、9的变化

目的 了解免疫受损大鼠铜绿假单胞菌肺部感染前后肺组织中细胞间黏附分子（ICAM）-1、基质金属蛋白酶（MMP）-2和MMP-9的改变及其与肺部炎症反应和肺损伤的关系。方法 建立免疫受损大鼠铜绿假单胞菌肺部感染的模型，观察其肺部炎症反应，测定湿／干比和支气管肺泡灌洗液中总蛋白（TP）了解肺损伤情况，对其肺组织分别行ICAM-1、MMP-2和MMP-9免疫组织化学研究。结果 1．铜绿假单胞菌肺部感染后，两组大鼠肺泡上皮细胞中ICAM-1染色强度较未感染时增加，接种后6h、9h、24h明显高于接种前（P〈0．05）；2．两组大鼠在铜绿假单胞菌肺部感染肝，肺组织中MMP-2染色增强，于接种后6h或9h达高峰，并持续至24h。两组大鼠感染前后MMP-2在各组织结构中的积分差异无统计学意义。MMP-9在感染前后的改变与MMP-2相仿；3．两组大鼠组织中ICAM-1积分与中性粒细胞半定量计数具有相关性（对照组rs=0．64l，P=0．001，免疫受损组rs=0．668，P〈0．001）；4．两组大鼠肺组织中MMP-2、MMP-9染色积分与PMN平定量计数呈正相关（P〈0．01）；5．免疫受损组大鼠支气管上皮细胞中MMP-9染色强度积分与TP具相关性（rs=0．434，P〈0．05），肺泡上皮细胞、小血管内皮细胞及内皮下组织中MMP-2染色强度与TP皆具相关性（rs分别为0．457、0．492、0．429，P00．05）。结论 免疫受损大鼠肺部铜绿假单胞菌感染后，肺组织中ICAM-1、MMP-2、MMP-9免疫组织化学显示染色增强，于感染后6～9h达高峰，与免疫受损大鼠肺组织中明显的中性粒细胞浸润及严重的肺损伤有关。     

紫杉醇联合奥沙利铂治疗胃癌21例

[目的]观察紫杉醇联合奥沙利铂治疗胃癌的疗效。[方法]将胃癌患者分为3组,分别采取奥沙利铂联合5-氟尿嘧啶(5-FU)、紫杉醇联合5-Fu及紫杉醇联合奥沙利铂治疗,观察治疗效果和不良反应。[结果]奥沙利铂联合5-Fu、紫杉醇联合5-Fu及紫杉醇联合奥沙利铂组治疗的总有效率分别为35.29%、36.84%和52.38%,后组与前2组比较P0.05;不良反应主要是血液学毒性、恶心呕吐、末梢神经感觉异常及脱发。[结论]紫杉醇联合奥沙利铂治疗胃癌疗效明显,不良反应在耐受范围之内,安全性好,值得临床推广应用。     

多西紫杉醇联合顺铂治疗乳腺癌肺转移32例的临床观察

目的观察多西紫杉醇联合顺铂治疗乳腺癌肺转移的临床疗效和毒副作用。方法32例乳腺癌肺转移患者，多西紫杉醇2550mg／m^2，静脉滴注1小时，第1、8、15日给药；顺铂20mg／m^2，第2～4日。28天为1个周期，完成2个周期后评价疗效。化疗前1天口服地塞米松8mg，2次／天，连服三天以防水潴留。结果32例患者完全缓解（CR）10例（31．2％），部分缓解（PR）11例（34．5％），稳定（SR）7例（21．8％），进展（PD）4例（12．5％），总有效率（CR＋PR）65．7％。不良反应主要是骨髓抑制及胃肠道反应，对症处理获得缓解。结论多西紫杉醇联合顺铂治疗肺转移性乳腺癌疗效较好，不良反应患者能耐受。     

雷替曲塞联合奥沙利铂与5-氟尿嘧啶联合顺铂方案治疗晚期胃癌的临床观察

目的 观察雷替曲塞联合奥沙利铂（L-OHP）治疗晚期胃癌的近期疗效和毒性.方法 将80例晚期胃癌患者分为两组,A组40例,给予雷替曲塞3 mg/m2,静脉滴注15分钟,d1;奥沙利铂130 mg,/m2,静脉滴注2小时,d1,3周重复1次.B组患者40例,给予5-氟尿嘧啶（5-FU）750 mg/m2,静脉滴注,d1 ～5;顺铂25 mg/m2,静脉滴注,d1 ～3,28天重复1次.结果 A、B两组患者的有效率分别为47.5％和22.5％,两组比较差异有统计学意义（P＜0.05）.不良反应主要是骨髓抑制和消化道反应.结论 与5-FU联合顺铂的方案比较,雷替曲塞联合奥沙利铂治疗晚期胃癌临床疗效较好,不良反应轻.     

紫杉醇联合化疗治疗复发的晚期非小细胞肺癌40例临床研究

目的 初步探讨紫杉醇联合化疗治疗一线化疗失败的晚期非小细胞肺癌的疗效。方法 40例复治患者，每周紫杉醇方案4例，紫杉醇60mg／m2／3h第1、8、15天，顺铂75mg／m^2第2天，每4周为周期；常规化疗组36例，紫杉醇135mg／m^2／3h第1天，顺铂75mg／m^2或卡铂300～350mg／m^2静脉输注第2天，每3-4周为1周期，进行24周期。结果 40例患者3例死亡未评价疗效，1例因毒副反应未完成治疗，总有效率13．9％(5／36)。肿瘤相关症状改善率58.3％(21／36)，随访27例生存期26．4周。1年生存率8％。主要毒副反应是骨髓抑制、肌肉、关节疼痛。结论 紫杉醇二线治疗有一定疗效并能改善症状，但地位尚需明确。     

海水吸入型肺损伤中蛋白激酶SPAK的表达改变

目的通过复制海水吸入引起的大鼠急性肺损伤模型,观察海水刺激对肺部炎症因子分泌、肺组织病理改变及肺组织中SPAK表达的影响。 方法将健康雄性SD大鼠分为正常组,海水处理1 h组,海水处理3 h组,海水处理6 h组,海水处理12 h组。经气管滴注无菌海水复制海水吸入性肺损伤模型,并按照预设时间收集组织标本并检测肺组织湿干比、病理、炎性因子TNF-α、IL-1β以及SPAK的转录、翻译改变。 结果海水吸入可以即刻引起血氧分压下降和二氧化碳分压升高,病理结果显示肺泡结构遭到破坏,肺泡壁断裂、增厚,中性粒细胞浸润,红细胞漏出等。ELISA结果显示海水刺激可引起肺内细胞分泌炎症因子TNF-α、IL-1β。海水吸入后SPAK蛋白表达明显增加,最高可达2.7倍左右(P<0.01),然后随着肺损伤病情的恢复,SPAK表达量逐渐下降。免疫组化染色结果显示海水吸入后SPAK表达明显升高,且广泛分布于细胞浆及细胞核。 结论在高渗透压海水的刺激下肺组织细胞可以通过转录和翻译使SPAK表达增多,进而参与肺损伤时的炎症反应,加重了肺损伤程度。     

布地奈德混悬液联合特布他林雾化液吸入治疗咳嗽变异性哮喘30例

目的探讨布地奈德混悬液联合特布他林雾化吸入治疗咳嗽变异性哮喘的临床疗效。方法将30例咳嗽变异性哮喘患者随机分成治疗组15例与对照组15例，对照组给予布地奈德混悬液雾化吸入治疗，其中6岁以下0．5mg／次，6岁以上1mg／次，每日2次。治疗组在对照组的基础上再给予特布他林雾化液联合吸入治疗，体重20kg以下2．5mg／次，20kg以上5mg／次，每日2次。观察两组的疗效及不良反应。结果总有效率：治疗组93．3％，对照组的75％，两组比较差异有统计学意义（X2=9．81，P〈0．01）。结论布地奈德混悬液联合特布他林雾化吸入治疗咳嗽变异性哮喘疗效满意。     

普拉格雷对海水吸入型急性肺损伤的作用分析

目的探讨海水吸入型急性肺损伤中血小板与中性粒细胞的黏附情况,以及普拉格雷对其的干预作用。 方法SD大鼠随机分为海水吸入1、2 h两个大组,组内随机分为空白对照组、海水处理组、溶剂处理组与普拉格雷处理组,每组8只大鼠。海水处理组在大鼠气管内灌注海水,溶剂处理组和普拉格雷处理组在海水处理之前4 h分别给予羟甲基纤维素钠溶液(CMC-Na)和普拉格雷灌胃处理。分别进行各组的病理切片HE染色,检测各组肺组织湿干比、血浆中炎症因子浓度,流式细胞术下检测血小板活化率以及与中性粒细胞的黏附情况,并进行肺泡灌洗液蛋白浓度测定以及髓过氧化物酶(MPO)活性测定。 结果与正常对照组比较,气管内滴入海水后大鼠肺部组织出现明显炎症和水肿,HE染色显示其组织结构紊乱,肺泡间质充血水肿,并有大量炎症细胞浸润,肺泡间隔明显增厚,ELISA法测得全身炎症因子,如TNF-α、IL-1β以及TXB2的表达增高,血小板与中性粒细胞黏附率显著增加,肺泡灌洗液蛋白定量以及MPO活性增加,并且海水吸入2 h较1 h各项指标增高更为显著。普拉格雷干预可显著减轻海水导致的肺组织损伤,减轻肺组织结构紊乱与炎症细胞浸润,减少炎症因子TNF-α、IL-1β以及TXB2的释放,并且抑制血小板的活化以及与中性粒细胞的黏附。 结论海水吸入型急性肺损伤中血小板与中性粒细胞的黏附率明显升高,普拉格雷可能通过降低此指标对肺损伤产生保护作用。     

环磷酰胺节律化疗抗肿瘤肺转移的作用及机制

荷瘤小鼠建模成功后，分别将35mg／kg环磷酰胺（CTX）（CTX节律组）、150mg／kgCTX（MTD组）、35mg／kgCTX＋150mg／kg CTX（联合组）、生理盐水（对照组）注入小鼠体内，观察各组小鼠肺转移情况，用免疫组化法检测各组瘤组织基质金属蛋白酶9（MMP-9）和趋化因子受体4（CXCR4）的表达及微血管密度（MVD）。结果CTX节律组和联合组肺转移率、瘤质量、MVD、CXCR4及MMP-9的表达均低于对照组和MTD组（P均〈0．05）。提示CTX节律化疗可明显抑制小鼠肺癌的血管生成和远处转移，其可能通过下调瘤组织MMP-9和CXCR4的表达而发挥作用。     

紫杉醇联合顺铂治疗晚期非小细胞肺癌的临床观察

目的观察紫杉醇(PTX)加顺铂(CDDP)联合化疗治疗晚期非小细胞肺癌的近期疗效及毒副反应。方法PTX135~175mg/m2静脉滴注,第1天;CDDP75mg/m2,分三次用完。每21天为1个周期,连用2或3周期。结果可评价疗效者37例,其中PR16例,总有效率为43.2%。毒副反应主要是骨髓抑制和恶心呕吐。结论PTX DDP治疗晚期非小细胞肺癌可获得较高疗效,毒副反应轻,是一个较好的联合化疗方案。     

Cryptogenic organizing pneumonitis during oxaliplatin chemotherapy for colorectal cancer: case report

The patient presented here is a 30-year-old woman who underwent anterior resection for the initial treatment of rectal cancer. A postoperative study showed a single liver metastasis. The patient received adjuvant pelvic radiotherapy with concomitant 5-fluorouracil (5-FU) treatment followed by liver metastasectomy 6 weeks after the completion of radiation therapy and chemotherapy. Adjuvant therapy with 5-FU, leucovorin, and oxaliplatin (FOLFOX 4 regimen) was continued. The initial five cycles were well tolerated with the occurrence of only paresthesia that did not interfere with function. After the sixth cycle of the treatment, progressive dyspnea and persistent cough developed in the patient, although her clinical history was negative for lung disease. A chest radiograph revealed diffuse bilateral interstitial infiltrates, and a chest CT scan showed bilateral alveolar infiltrates predominant in the right lung. Lung biopsy by video-assisted thoracoscopy was performed, and the histologic report showed cryptogenic organizing pneumonitis (COP). Prednisone therapy (1 mg/kg/d) resulted in a very good clinical response. In fact, the patient had complete remission of respiratory symptoms including cough and dyspnea after 4 days of treatment, and the chest CT scan showed complete resolution of lung infiltrates after 4 weeks. One month later, the patient continued adjuvant treatment with six cycles of 5-FU, leucovorin, and irinotecan (ie, the FOLFIRI regimen) without complications. Thus, oxiplatin was implicated as the likely cause of this drug-induced lung toxicity, which is a very rare complication associated with platins. Diffuse interstitial lung disease, particularly COP, has been described following the administration of the cytotoxic agents bleomycin and busulfan, but a connection to oxaliplatin has not been reported before this case.     

A phase I study of combination of intravenous gemcitabine, oxaliplatin, and 5-FU with daily oral thalidomide (GOFT) in metastatic/locally advanced pancreatic carcinoma patients

BACKGROUND/AIMS: The phase I study was to determine the maximum tolerance dose and dose-limiting toxicity of gemcitabine/oxaliplatin/5-FU/thalidomide (GOFT) in patients with advanced pancreatic cancer. METHODOLOGY: Chemotherapy-naive patients with histologically proven locally advanced or metastatic pancreatic cancer were enrolled. Gemcitabine was given in a 1-hour infusion followed by oxaliplatin in a 2-hour infusion on day 1, and 5-FU in a 24-hour infusion on day 2, and oral thalidomide 100mg was given daily after intravenous chemotherapy. This regimen was given every 2 weeks. Dose levels of regimen were: level I: gemcitabine 1000mg/m2 + oxaliplatin 60mg/ m2 + 5-FU 1000mg/m2 + thalidomide 100mg/day, level II: gemcitabine 1000mg/m2 + oxaliplatin 70mg/m2 + 5-FU 1000mg/m2 + thalidomide 100mg/day, level III: gemcitabine 1250mg/m2 + oxaliplatin 60mg/m2 + 5-FU 1000mg/m2 + thalidomide 100mg/day. The NCI-CTC grade 3/4 toxicity was used for dose-limiting toxicity. Maximum tolerance dose was determined after the first two cycles in each patient. RESULTS: There were 6 patients in level I, 6 patients in level II, and 1 patient in level III. One of the 6 patients had DLT in level I (grade 3 infection and vomiting), 2 of 6 patients had DLT in level II (grade 3 leukopenia) and 1 patient in level III had DLT (grade 3 leukopenia and stomatitis). Other toxicities at level I/II were grade 1/2 leukopenia (7 episodes), grade 1/2 anemia (5), grade 1/2 nausea (5), grade 1 diarrhea (2), grade 1 alopecia (2), grade 1 skin (2), grade 1 allergy (1). CONCLUSIONS: The GOFT regimen was well tolerated and showed good treatment effect on the pancreatic cancer. We recommended the dose of level II GOFT regimen for further phase II trial.     

Effects of inducible nitric oxide synthase inhibition in bronchial vascular remodeling-induced by chronic allergic pulmonary inflammation

Vascular remodeling is an important feature in asthma pathophysiology. Although investigations suggested that nitric oxide (NO) is involved in lung remodeling, little evidence established the role of inducible NO synthase (iNOS) isoform in bronchial vascular remodeling. The authors investigated if iNOS contribute to bronchial vascular remodeling induced by chronic allergic pulmonary inflammation. Guinea pigs were submitted to ovalbumin exposures with increasing doses (1～5 mg/mL) for 4 weeks. Animals received 1400W (iNOS-specific inhibitor) treatment for 4 days beginning at 7th inhalation. Seventy-two hours after the 7th inhalation, animals were anesthetized, mechanical ventilated, exhaled NO was collected, and lungs were removed and submitted to picrosirius and resorcin-fuchsin stains and to immunohistochemistry for matrix metalloproteinase-9 (MMP-9), tissue inhibitor of metalloproteinase-1 (TIMP-1), and transforming growth factor-β (TGF-β). Collagen and elastic fiber deposition as well as MMP-9, TIMP-1, and TGF-β expression were increase in bronchial vascular wall in ovalbumin-exposed animals. The iNOS inhibition reduced all parameters studied. In this model, iNOS inhibition reduced the bronchial vascular extracellular remodeling, particularly controlling the collagen and elastic fibers deposition in pulmonary vessels. This effect can be associated to a reduction on TGF-β and on metalloproteinase-9/TIMP-1 vascular expression. It reveals new therapeutic strategies and some possible mechanism related to specific iNOS inhibition to control vascular remodeling.     

Weekly oxaliplatin, high-dose infusional 5-fluorouracil and folinic acid as palliative third-line therapy of advanced colorectal carcinoma

The efficacy of oxaliplatin combined with high-dose 5-fluorouracil (5-FU) and folinic acid (FA) as an outpatient salvage treatment for patients with metastasized colorectal cancer was retrospectively analyzed in one center. Tumor progression had occurred for the majority of patients during two regimens (n = 11) otherwise during one (n = 1) regimen of prior 5-FU-based chemotherapy, which had been applied in a standardized sequential fashion. As third-line therapy oxaliplatin was infused intravenously over 2 h at a dose of 60 mg/m2 prior to a 2-h infusion of FA (500 mg/m2). 5-FU (2,600 mg/m2) was subsequently given over 24 h. A favorable response was observed in 9/12 (75%) of the heavily pretreated patients, including partial remissions in 3/12, minor responses in 2/12 and stable disease in 4/12 patients. The median progression free time was 23 weeks (interquartile range i. r. 0-28) for all patients, the median survival time from start of third-line therapy 55 weeks (i. r. 40-86). The median survival time from the beginning of first-line palliative chemotherapy was 34 months (i. r. 25-45 months). The highest toxicity was WHO grade III and was observed in six patients: Nausea (2), diarrhea (3), vomiting (2) and peripheral neuropathy (1). The quality of life was not adversely affected by the oxaliplatin/5-FU/FA-regimen as assessed by the EORTC QLQ-C30 questionnaire. Thus, the results show the efficiency and low toxicity of oxaliplatin/high-dose 5-FU/FA as palliative third-line therapy of patients with metastasized colorectal cancer and emphasize that sequential palliative chemotherapy may lead to extended survival of these patients.     

Inhalation administration of all-trans-retinoic acid for treatment of elastase-induced pulmonary emphysema in Fischer 344 rats

A past study demonstrated that all-trans-retinoic acid (ATRA) treatment by intraperitoneal injection in a rat model of elastase-induced emphysema caused tissue regeneration as evidenced by a decrease in alveolar size and lung volume and an increase in alveolar number. We postulated that treatment with this retinoid by nose-only inhalation exposure would be a more efficient means of targeting damaged lung tissue. Emphysema was induced in male Fischer 344 rats by intratracheal instillation of pancreatic elastase (0.5 IU/g body weight). Four weeks after elastase instillation, animals were treated once daily, 4 days/week, for 3 weeks by exposing them nose-only to aerosolized ATRA (target concentration-time of 3000 or 15,000 mg-min/m3) or by injecting them intraperitoneally with ATRA in cottonseed oil (0.5 or 2.5 mg/kg). Based on estimates of particle deposition in the respiratory tract, inhalation doses were chosen to be consistent with injected doses. Lungs were fixed by inflation with formalin (constant pressure for 6 hours followed by >48 hours of immersion) and were embedded in paraffin. Sections were evaluated by histopathology and stereology. Inhalation exposure to ATRA at both aerosol concentrations caused significant elevations of ATRA in the lung, whereas only the high-dose injection treatment was associated with an elevation of lung ATRA. The mean ATRA concentration from lungs of rats in the high-dose inhalation exposure groups as measured by liquid chromatography--mass spectrometry was approximately 12-fold greater than that of high-dose injection-treated rats. Elastase instillation caused increased lung volumes, irregular alveolar air space enlargement, and fragmentation and attenuation of alveolar septa. Neither inhaled nor injected ATRA reduced the enlarged lung volumes associated with this emphysema model. Stereology demonstrated that alveolar air space enlargement in ATRA-treated rats was similar to that in sham-treated emphysematous animals. Thus, while inhalation treatment caused greater levels of the drug in lung tissue in comparison to that of injection-treated animals, treatment with ATRA by either route of administration did not cause a reversal of lung tissue damage in this model of elastase-induced emphysema.     

己酮可可碱对心肌肥厚大鼠基质金属蛋白酶2和9表达的影响

目的观察基质金属蛋白酶2和9在心肌肥厚大鼠模型中的变化,并采用己酮可可碱进行干预,以确定己酮可可碱对基质金属蛋白酶的影响及其在心肌肥厚过程中的作用。方法24只雄性SD大鼠随机分为对照组、去甲肾上腺素造模组(模型组)和去甲肾上腺素 己酮可可碱组(治疗组)。采用VG染色评价组织胶原表达,并测定心肌组织胶原含量,免疫组织化学法检测心肌组织基质金属蛋白酶2和9的蛋白表达。结果模型组大鼠发生左心室肥厚,胶原含量显著高于对照组(1.929±0.514mg/g比1.009±0.442mg/g,P<0.01);基质金属蛋白酶2和9表达(分别为131.1±9.8、125.3±4.1)显著低于对照组(P<0.01)。己酮可可碱治疗组心肌总胶原含量较模型组显著降低(1.151±0.215mg/g,P<0.01);基质中基质金属蛋白酶2和9的表达(分别为153.5±6.9、149.5±5.3)较模型组显著增高(P<0.01)。结论己酮可可碱能有效防治心肌肥厚的发生及细胞外基质重塑,这一效应可能与其降低心肌组织中基质金属蛋白酶2和9的高表达有关。     

阿托伐他汀对心肌肥厚大鼠细胞外基质重塑的抑制作用

目的探讨阿托伐他汀对去甲肾上腺素诱导的心肌肥厚大鼠细胞外基质重塑的影响及其可能的机制.方法雄性SD大鼠随机分为三组(1)对照组,(2)去甲肾上腺素组[1.06 mg/(kg·d)×15 d],(3) 去甲肾上腺素+阿托伐他汀组[50 mg/(kg·d)×15 d].去甲肾上腺素ip,2次/d,15 d,建立心肌肥厚模型.应用超声心动图及病理学方法评价整体心肌肥厚及组织胶原表达.用逆转录-聚合酶链反应法(RT-PCR)及免疫组化检测细胞外基质调节因子-基质金属蛋白酶(MMP-9)及其生理性抑制剂(TIMP-1)和转化生长因子β1(TGF-β1)mRNA和蛋白表达.结果去甲肾上腺素组大鼠发生左心室肥厚及纤维化,胶原含量及MMP-9、TIMP-1和TGF-β-1蛋白、mRNA表达显著高于健康对照组(P<0.01).阿托伐他汀能减少心肌中总体胶原及Ⅰ、Ⅲ型胶原的合成及MMP-9、TGF-β-1表达(P<0.01).结论 MMP-9、TIMP-1和TGF-β-1与心肌肥厚大鼠的细胞外基质重塑有关.阿托伐他汀能有效防治心肌纤维化及细胞外基质重塑,这一效应与其降低心肌中高表达的MMP-9和TGF-β-1有关.     

Oxaliplatin combined with 5-FU in second line treatment of advanced pancreatic adenocarcinoma. Results of a phase II trial

BACKGROUND: The efficacy and benefit of second-line chemotherapy in advanced pancreatic adenocarcinoma has never been demonstrated although it is regularly used. PATIENTS AND METHODS: A randomized phase II study evaluating oxaliplatin alone (OXA), infusional 5-fluorouracil alone (5-FU) and an oxaliplatin/infusional 5-FU combination (OXFU) in untreated advanced pancreatic adenocarcinoma has been conducted. In this trial, a second-line treatment with the OXFU regimen (OXA 130 mg/m2 2-h intravenous (i.v.) infusion combined with 5-FU (1000 mg/m2/day, continuous i.v., days 1-4), every 3 weeks) was offered to patients progressing after single agent treatment. RESULTS: Eighteen out of 32 patients (12 males, median age 57 years) treated in the single agent arms received the OXFU combination in second-line treatment. WHO performance status was at least 2 in 61% of the patients. There was no objective response and 3 patients (17%) had a disease stabilisation. Median time to progression from the start of second-line treatment was 0.9 months. Median overall survival was 4.9 months from the start of front-line therapy and 1.3 months from the start of second-line therapy. CONCLUSION: The results of this trial bring arguments to support a modest value of second-line chemotherapy for advanced pancreatic adenocarcinoma.     

维A酸受体β在食管鳞癌组织中的表达及其与化疗疗效的关系

目的 观察维A酸受体β(RAR-β)在食管鳞癌中的表达及其与化疗疗效的关系.方法 52例中晚期食管鳞癌患者给予以顺铂(DDP)+5-氟尿嘧啶(5-FU)为基础的联合方案化疗.DDP 80 mg/m2,分为5 d静脉滴注;5-FU每日375 mg/m2,第1～5天静脉滴注,21 d为1个周期.应用免疫组化法检测RAR-β在食管鳞癌组织中的表达.以50例正常食管黏膜作为对照.结果 RAR-β阳性染色主要位于细胞质和(或)胞核,食管鳞癌组织中RAR-β阳性率(61.5%,32/52)明显低于正常食管黏膜组织(92.0%,46/50),P＜0.05.52例食管鳞癌患者共完成228个化疗周期,总有效率71.2%,RAR-β阳性表达者有效率84.4%(27/32),显著高于RAR-β阴性表达者的50.0%(10/20),P＜0.05.RAR-β阳性表达者中位疾病进展时间为5.9个月,中位生存时间12.1个月,2年生存率56.7%;而RAR-β阴性表达者中位疾病进展时间为2.1个月,中位生存时间5.8个月,2年生存率32.9%,两组间比较差异均有统计学意义(P＜0.05).结论 免疫组化法检测RAR-β的表达可作为临床上预测食管癌化疗疗效及预后的指标之一,同时RAR-β可能成为食管癌治疗的靶点.