肺癌患者血管紧张素转换酶变化的观察

目的　研究肺癌患者血清血管紧张素转换酶(SACE)的活性及其化疗后的变化。方法　用紫外线分光光度计测定肺癌患者、肺炎患者及正常人的SACE。结果　肺癌患者的SACE活性明显低于肺炎组及正常组(P<0.01)。肺癌患者经化疗后SACE活性明显增高(P<0.01)。结论　测定SACE活性有助于肺部良、恶性病变的鉴别诊断及监测肺癌预后     

肺癌患者血管紧张素转换酶变化的观察

目的 研究肺癌患者血清血管紧张素转换酶（ＡＳＣＥ）的活性及其化疗的的变化。方法 用紫外线分光光度计测定肺癌患者、肺炎患者及正常人的ＳＡＣＥ。结果 肺癌口才的ＳＡＣＥ活性明显低于肺炎组及正常组（Ｐ〈０．０１）。肺癌患者经化疗后ＳＡＣＥ活性明显增高（Ｐ〈０．０１）。结论 测定ＳＡＣＥ活性有助于肺部良、恶性病变的鉴别诊断及监测肺癌预后。     

肺癌患者血管紧张素转换酶变化的观察

目的 对１００例肺癌,６８例肺炎,７２例健康人的血清血管紧张素转换酶活性的评价,并对肺癌患者化疗前后ＳＡＣＥ活性变化进行了对比观察。方法 用紫外线分光光度测定血清中血管紧张素转换酶。结果 肺癌患者的血清血管紧张素转换酶活性明显低于肺炎组及健康组织。肺癌患者经化疗后ＳＡＣＥ活性增高。结论 血清中血管紧张素活性的测定,对肺癌予后的估价及肺部阴影的鉴别诊断可能有一定帮助     

肺癌和食管癌患者手术前后血清血管紧张素转换酶变化的观察

本文报道25例正常人,25例肺癌和25例食管癌病人血清血管紧张素转换酶(SACE)活性的测定结果。手术前肺癌患者的SACE活性明显低于其它组。正常人,食管癌和肺癌的SACE平均值分别为36.2±0.75,34.7±1.87和24.6±1.34u/ml。在手术中肺癌和食管癌组平均SACE活性明显降低,手术后3天肺癌组平均SACE活性较手术前增加,但与食管癌组相比仍较低;其中小细胞肺癌较其它类型肺癌更低。总结以上发现,我们认为SACE活性的测定对肺癌患者的预后估计及鉴别诊断有一定帮助。     

血管紧张素转换酶基因多态性与肺癌关系的研究

背景与目的血管紧张素转换酶(ACE)是RAS系统的关键酶,在肺内表达丰富。近年来的研究发现ACE有着广泛的生理作用,包括参与肿瘤发生和发展的病理过程。本研究拟探讨ACE基因内一287bp的片段插入(insertion,I)与缺失(deletion,D)多态性是否与肺癌的易感性、病理类型和临床分期存在相关性。方法从47例肺癌患者和54例正常对照者的外周静脉血中提取DNA,采用PCR方法测定基因型。结果肺癌组中II、ID和DD基因型频率分别为0.447、0.447和0.106,I和D等位基因的频率分别为0.670和0.330;正常对照组中II、ID和DD基因型频率分别为0.370、0.556和0.074,I和D等位基因的频率分别为0.648和0.352,两组间各基因型和等位基因的分布无显著统计学差异(P>0.05)。小细胞与非小细胞肺癌患者间以及各临床分期间也未发现ACE基因型和等位基因分布的差异(P>0.05)。结论本研究未发现ACE的基因多态性与肺癌的易感性、病理类型或临床分期存在相关性。     

肺癌X刀治疗后血管紧张素转换酶的变化

血管紧张素转换酶(SACE)在机体疾病状态下的变化在临床上已有广泛的研究。我们对46例肺癌患者X刀治疗前后的变化进行了观察,报告如下。 一、材料与方法 1.临床资料:实验组:经病理学确诊、住院行X刀治疗的     

结肠癌患者外周血血管紧张素转换酶基因多态性

目的 研究血管紧张素转换酶（ACE）基因多态性与结肠癌的关系。方法 采用聚合酶链反应（PCR）检测30例结肠癌患者和30例正常人外周血中ACE基因缺失型（DD型）、插入型（ID型）和Ⅱ型及I/D等位基因在结肠癌患者外周血中的分布规律。结果 结肠癌患者外周血中存在ACE基因插入/缺失（I/D）多态性,DD型、ID型和Ⅱ型3种基因型的占比分别为6.67%,36.67%,56.66%,I/D等位基因分布频率分别为93.33%和6.67%,健康对照组DD型、ID型和Ⅱ型3种基因型的占比分别为16.67%,53.33%,30.00%,I/D等位基因分布频率分别为83.33%和16.67%,经统计学分析,两组间DD型、ID型和Ⅱ型的分布频率差异有统计学意义(P<0.05),I/D等位基因分布频率差异无统计学意义(P>0.05)。结论 结肠癌患者外周血中存在ACE基因I/D多态性,Ⅱ型基因分布较健康对照组显著升高,预示与结肠癌发病存在一定关系。     

血管紧张素转换酶抑制剂抗肿瘤作用研究进展

血管紧张素转换酶抑制剂（ACEI）是临床上常用的抗高血压药物,近年来,越来越多的研究发现它们还具有抗肿瘤的作用,ACEI类药物可能通过抑制血管内皮生长因子（VEGF）、基质金属蛋白酶（MMP）的表达,增加血管抑素的生成等多个方面发挥其抗肿瘤作用。其临床相对优良的安全性可能为抗肿瘤治疗提供新的策略。     

血管紧张素转换酶抑制剂抗肿瘤作用研究进展

血管紧张紊转换酶抑制剂(ACEI)是临床上常用的抗高血压药物,近年来,越来越多的研究发现它们还具有抗肿瘤的作用,ACEI类药物可能通过抑制血管内皮生长因子(VEGF)、基质金属蛋白酶(MMP)的表达,增加血管抑素的生成等多个方面发挥其抗肿瘤作用。其临床相对优良的安全性可能为抗肿瘤治疗提供新的策略。     

Use of beta‐blockers,angiotensin‐converting enzyme inhibitors and angiotensin receptor blockers and breast cancer survival: Systematic review and meta‐analysis

Breast cancer (BC) is the second leading cause of cancer death among women in Western Countries. Beta‐blocker (BB) drugs, angiotensin‐converting enzyme inhibitors (ACEi) and angiotensin receptor blockers (ARB) were suggested to have a favorable role in the development and progression of BC. We have performed a meta‐analysis to clarify the potential benefits of these drugs on BC survival. A total number of 46 265 BC patients from eleven papers were included, ten independent studies on BB use and seven on ACEi/ARB use. The summary hazard ratio (SHR) was estimated by pooling the study‐specific estimates with random effects models and maximum likelihood estimation. We assessed the homogeneity of the effects across studies and evaluated between‐study heterogeneity by meta‐regression and sensitivity analyses. We found a significant improvement in BC specific survival for patients treated with BB drugs at the time of BC diagnosis (SHR: 0.44; 95%CI: 0.26–0.73 with I² = 78%). We also observed a borderline significant improvement in disease free survival for subjects treated with BB (SHR: 0.71, 95%CI: 0.19–1.03). No association of ACEi/ARB use with disease free and overall survival was found. In conclusion, we report epidemiological evidence that BB improve BC‐specific survival. Clinical trials addressing this hypothesis are warranted.     

Renin-angiotensin system inhibitors, angiotensin I-converting enzyme gene insertion/deletion polymorphism, and cancer: the Rotterdam Study

BACKGROUND: Angiotensin I-converting enzyme (ACE) inhibitors, angiotensin II antagonists, and the ACE insertion/deletion (I/D) gene polymorphism all influence serum angiotensin II action. Because angiotensin II levels have been associated with cancer, the objective of the current epidemiologic study was to investigate whether renin-angiotensin system inhibitors and/or ACE genotypes were associated with an altered risk of colorectal, lung, breast, and prostate cancer. METHODS: Data were obtained from the Rotterdam Study, a population-based, prospective cohort study with 7983 participants. Participants who had a history of 1 of the cancers of interest (n = 216) or who had a medication history <6 months (n = 88) were excluded, leaving 7679 participants, of whom the ACE genotypes could be assessed in 6670 individuals. The mean follow-up was 9.6 years, during which 730 incident cancers occurred. The effect of medication, ACE I/D genotypes, and their interaction on cancer risk and progression was studied by using Cox proportional hazard models. RESULTS: Carriers of the high-activity genotype DD had an increased risk of breast cancer compared with low-activity II/ID genotype carriers (hazard ratio [HR], 1.47; 95% confidence interval [95% CI], 1.05-2.04), but no association was demonstrated for other cancers. DD carriers who were exposed to long-term and high-dose medication were at lower risk for cancer (HR, 0.28; 95% CI, 0.10-0.79). Short-term, high-dose users were at risk for colorectal cancer progression in the II/ID stratum (HR, 3.83; 95% CI, 1.67-8.79). CONCLUSIONS: Renin-angiotensin system-inhibiting drugs seemed to protect against cancer in individuals with the DD genotype, which was associated with high levels of ACE.     

Inhibition of the renin–angiotensin system improves physiological outcomes in mice with mild or severe cancer cachexia

Cancer cachexia describes the progressive skeletal muscle wasting and weakness associated with many cancers. Cachexia reduces mobility and quality of life and accounts for 20–30% of all cancer‐related deaths. Activation of the renin–angiotensin system causes skeletal muscle wasting and weakness. We tested the hypothesis that treatment with the angiotensin converting enzyme (ACE) inhibitor, perindopril, would enhance whole body and skeletal muscle function in cachectic mice bearing Colon‐26 (C‐26) tumors. CD2F1 mice received a subcutaneous injection of phosphate buffered saline or C‐26 tumor cells inducing either a mild or severe cachexia. The following day, one cohort of C‐26 mice began receiving perindopril in their drinking water (4 mg kg^?1 day^?1) for 21 days. In mild and severe cachexia, perindopril increased measures of whole body function (grip strength and rotarod) and reduced fatigue in isolated contracting diaphragm muscle strips (p < 0.05). In severely cachectic mice, perindopril reduced tumor growth, improved locomotor activity and reduced fatigue of tibialis anterior muscles in situ (p < 0.05), which was associated with increased oxidative enzyme capacity (succinate deyhydrogenase, p < 0.05). Perindopril attenuated the increase in MuRF‐1 and IL‐6 mRNA expression and enhanced Akt phosphorylation in severely cachectic mice but neither body nor muscle mass was increased. These findings support the therapeutic potential of ACE inhibition for enhancing whole body function and reducing fatigue of respiratory muscles in early and late stage cancer cachexia and should be confirmed in future clinical trials. Since ACE inhibition alone did not enhance body or muscle mass, co‐treatment with an anabolic agent may be required to address these aspects of cancer cachexia.     

Serum ribonuclease in patients with lung carcinoma

Fifty-one previously untreated cases of lung carcinoma and 7 normal healthy controls were evaluated with respect to serum ribonuclease (S-RNase) levels. Cellular immunity was tested in 22 of these 51 cases by leukocyte migration inhibition test (MIT) using extract of culture cell line of lung carcinoma. S-RNase levels in lung carcinomas were significantly elevated. There appeared to be no difference in S-RNase levels by histological classification. More striking was high S-RNase level in disseminated versus localized cases. MIT results indicated impairment of cellular immunity in those cases of more elevated S-RNase. S-RNase may be implicated in blocking phenomenon associated with neoplastic disease.     

Importance of biologic status to the postoperative prognosis of patients with stage III nonsmall cell lung cancer

The prognosis of patients with stage III nonsmall cell lung cancer was studied, with special attention to their biologic status prior to lung resection. The biologic status was estimated from the neutrophil/lymphocyte ratio in the peripheral blood, serum albumin level, and erythrocyte sedimentation rate. Among 46 patients who underwent potentially curative operations, 31 cases of biologic status A or B (more than two parameters normal) revealed 37.6% of a 5-year survival rate, whereas there was no 5-year survivor in 15 cases of biologic status C or D (more than two parameters abnormal). Of the 5-year survival rate in T3N0 disease of biologic status A or B, the 60% surviving (of 10 cases) was in marked contrast to the same stage disease of biologic status C or D where only 1 patient (of 10 cases) was still surviving at more than 30 months. In 30 patients with T3N0, T3N1, and T2N2 diseases of biologic status A or B, where long-term survivors were derived, the 5-year survival rate in 30 patients of biologic status A or B was 36.6% in contrast to no long-term survivor in the same stage diseases of biologic status C or D (n = 25). We conclude that surgical results in stage III nonsmall cell lung cancer will be beneficial in patients of biologic status A or B, but nonbeneficial in patients with the same stage of biologic status C or D.