XRCC1表达对胃癌术后奥沙利铂化疗患者预后的影响

目的 观察XRCC1在胃癌组织中的表达,探讨其与接受手术及奥沙利铂化疗患者预后的影响.方法 选择接受手术和术后行奥沙利铂化疗的胃癌患者的组织标本,采用免疫组化(SP)法检测XRCC1的表达,Log-rank分析其与临床特征和远期生存率的关系.结果 胃癌组织中XRCC1阳性率为55.6%.XRCC1表达阴性患者中位生存期为52个月,3年生存率为71.9%,5年生存率为34.4%;而XRCC1表达阳性的患者中位生存期为42.4个月,3年生存率为52.5%,5年生存率为22.5%(χ2=0.756,P=0.038 4).结论 胃癌组织中的XRCC1表达水平与接受手术及术后奥沙利铂化疗患者的远期生存率密切相关,可作为术后胃癌生存预测的指标.     

奥沙利铂化学治疗方案在结直肠癌术后辅助治疗的疗效和安全性比较

目的 比较5-氟尿嘧啶+亚叶酸钙联合奥沙利铂(FOLFOX4/6)方案与卡培他滨联合奥沙利铂(XELOX)方案在进展期结直肠癌术后辅助化学治疗中的疗效和安全性.方法 回顾性分析286例进展期结直肠癌患者的术后临床资料,其中204例给予FOLFOX4/6方案术后辅助化学治疗,82例给予XELOX方案术后辅助化学治疗,比较两组患者的3年无病生存率、3年总生存率和不良反应发生情况.两组计数资料比较采用x2检验,计量资料比较采用t检验.结果 FOLFOX4/6方案组完成12个周期化学治疗的患者153例(75％),XELOX方案组完成8个周期化学治疗的患者66例(80％).两组患者的3年无病生存率(FOLFOX4/6组临床Ⅱ期患者为87％,Ⅲ期患者为82％;XELOX组Ⅱ期83％,Ⅲ期80％)和总生存率(FOLFOX4/6组Ⅱ期92％,Ⅲ期88％;XELOX组Ⅱ期89％,Ⅲ期86％)差异均无统计学意义(P均＞0.05).FOLFOX4/6和XELOX组患者各种常见不良反应的总发生率差异无统计学意义(P＞0.05),以Ⅰ和Ⅱ度不良反应多见,Ⅲ和Ⅳ度不良反应非常少见.Ⅲ和Ⅳ度不良反应中,FOLFOX4/6组患者中性粒细胞减少的发生率稍高于XELOX组,而XELOX组患者手足综合征的发生率稍高于FOLFOX4/6组,但差异均无统计学意义(x2=0.060、0.928,P均＞0.05).结论 FOLFOX4/6与XELOX方案作为进展期结直肠癌术后辅助化学治疗的疗效无明显差异,患者基本可以耐受不良反应,安全性较好.     

EMX2和β-catenin Cyclin D1在结直肠癌组织中的表达及临床意义

目的观察空通气孔同源框2(EMX2)和β-连环蛋白(β-catenin)、细胞周期蛋白D1(Cyclin D1在正常结直肠黏膜、结直肠癌组织中的表达情况,探讨结直肠癌发展过程中EMX2与β-catenin、Cyclin D1的关系。方法 S-P法检测EMX2和β-catenin、Cyclin D1在正常结直肠黏膜、结直肠癌组织中蛋白表达情况,并分析EMX2和β-catenin、Cyclin D1与结直肠癌临床病理特征之间及患者预后的关系。结果 (1)在正常结直肠黏膜、结直肠癌组织中EMX2阳性表达率分别为76. 7%和38. 2%(P 0. 01),EMX2阳性表达率与结直肠癌临床分期及淋巴结转移有关。在正常结直肠黏膜、结直肠癌组织中β-catenin阳性表达率分别为6. 7%、65. 5%; Cyclin D1阳性表达率分别为10. 0%、63. 6%。β-catenin与Cyclin D1阳性表达率与结直肠癌的临床分期、肿瘤分化程度、淋巴结转移有关(P 0. 05)。(2)在结直肠癌组织中EMX2和β-catenin表达呈负一致性(Kappa值=-0. 389,P=0. 000); EMX2与Cyclin D1表达一致性不明显(Kappa值=-0. 161,P=0. 054)。(3)应用Kaplan-Meier生存分析表明,结直肠癌组织中EMX2阳性表达与患者较好的预后有关(P=0. 032)。结论结直肠癌组织中EMX2阳性表达减少,EMX2低表达与结直肠癌患者的临床分期、淋巴结转移及预后密切相关。在结直肠癌患者中检测EMX2,可能成为判断患者临床分期和预后指标。     

胃癌组织中乳腺癌易感基因1表达状况与奥沙利铂方案辅助化疗疗效、预后的相关性

目的:探讨胃癌组织中乳腺癌易感基因1(breast cancer susceptibility gene 1,BRCA1)表达状况,并分析其与奥沙利铂方案辅助化疗疗效、预后的相关性.方法:选取武警四川总队医院2010-01/2011-12间110例胃癌根治术后奥沙利铂方案辅助化疗患者为研究对象,采取免疫组织化学方法测定胃癌组织中BRCA1表达,分析BRCA1表达与患者的临床疗效与预后的相关性.结果:BRCA1表达阳性vs阴性治疗有效率35.9%vs 60.6%,差异有统计学意义(P0.05);BRCA1表达阳性vs阴性患者3年无病生存(disease-free survival,DFS)率和总生存(overall survival,OS)率(30.8%vs 56.3%)、(3 8.5%vs 6 4.8%),差异有统计学意义(P0.05).结论:胃癌组织中BRCA1表达可以作为胃癌根治术后患者奥沙利铂方案辅助化疗疗效的预测指标,也可作为预后观察的重要指标.     

中国人结直肠腺癌雌激素受体β的表达

目的:确定ER β在中国人结直肠癌中的表达特点.方法:采用免疫组织化学方法对40例结直肠癌进行了ER β检测,10例结肠腺瘤以及10例正常结肠活检标本作为对照组也进行了ER β检测.结果:ER β在正常人结肠黏膜、结肠腺瘤以及结直肠癌组织中均有不同程度的表达,正常结肠黏膜(2/10)和结肠腺瘤组织(3/10)主要表现为上皮及腺体细胞核及核周胞质染色,而结直肠癌呈弥漫性胞质染色,其中约57.5%CRCs患者核染阳性率大于10%.ER β阳性和阴性组与肿瘤浸润深度、淋巴结转移以及生存率无明显相关.结论:结直肠癌组织中存在大量的ER β阳性细胞;部分正常结肠黏膜也存在ER β的表达;ER β在正常人结肠黏膜、结肠腺瘤细胞以核及核周胞质染色为主,而结直肠癌组织以上弥漫性胞质染色为主.     

解聚素-金属蛋白酶17在锯齿状结直肠癌中的表达及其意义

目的检测ADAM17在锯齿状结直肠癌组织和正常组织中的表达,初步探讨ADAM17在锯齿状癌变途径中的作用机制。方法回顾性分析2016年4月至2018年4月期间我院行结肠镜或手术所取得的病理标本120例,其中结直肠癌组织60例,正常结直肠黏膜组织60例,采用RT-PCR和免疫组化法检测ADAM17在结直肠癌及正常结直肠黏膜组织中的表达情况,分析ADAM17在结直肠癌组织中的表达和临床病理特征之间的关系。结果在结直肠癌组织中ADAM17表达的阳性率为75.0%(45/60),在正常黏膜组织中ADAM17的阳性率为21.7%(13/60),差异具有统计学意义(P 0.001)。ADAM17主要表达在细胞内和基底外侧质膜上。在正常结肠黏膜中,ADAM 17在隐窝上皮细胞、血管、黏膜肌和固有肌细胞中表达。结直肠癌组织中ADAM17的相对表达量显著高于正常黏膜组织(0.65±0.2和0.29±0.1,P 0.001)。ADAM17在结直肠癌组织中的表达水平与肿瘤浸润深度(P 0.001)、血管侵犯(P=0.001)、淋巴侵犯(P=0.001)、远处转移(P=0.001)相关。结论 ADAM17在结直肠癌中高表达,并与肿瘤的浸润深度、血管侵犯、淋巴转移以及远处转移密切相关。表明ADAM17可能是结直肠癌的一个有前途的治疗靶点和预测性生物标记物。     

PTEN和Cdx2在溃疡性结肠炎和结直肠癌中的表达

PTEN具有磷酸酶活性，能调控细胞的增殖、迁移和凋亡。Cdx2是一种肠道特异性转录因子，在调节肠上皮细胞分化、增殖中起关键作用。近年溃疡性结肠炎（UC）与结直肠癌之间的关系日益受到关注。目的：观察UC和结直肠癌组织中PTEN和Cdx2的表达，探讨两者在UC癌变进程中的作用。方法：在上海瑞金医院1997年1月-2007年10月诊断的UC患者中收集经病理检查确诊者的蜡块标本，其中UC组17例，UC相关结直肠癌组7例，另收集非UC相关结直肠癌标本35例和正常肠黏膜标本15例，以免疫组化方法检测PTEN和Cdx2表达。结果：PTEN和Cdx2在正常结直肠组织中基本呈阳性表达．阳性率分别为93.3％和100％，UC组织两者表达阳性率显著降低，均仅为6.7％。UC相关结直肠癌组PTEN和Cdx2表达阳性率显著低于非UC相关结直肠癌组（PTEN：28．6％对83．9％，Cdx2：42．9％对90．3％，P〈0．01）。结论：UC与结直肠癌之间可能存在相关性。PTEN和Cdx2在调控肠上皮分化、增殖的过程中可能有相似的调节点或具有协同作用，两者可能共同参与了对UC癌变进程的调控。     

Smad4表达异常与结直肠癌的相关性研究

目的 探讨结直肠组织Smad4 mRNA及其蛋白表达水平变化、Smad4基因CpG岛异常甲基化与结直肠癌及其临床病理特征的关联性.方法 应用RT-PCR方法及测序、半定量RT-PCR方法、甲基化特异性PCR(MSP)技术和免疫组织化学方法,各自检测43例患者的结直肠癌组织、癌旁组织及30例结直肠腺瘤组织、12例健康人结肠黏膜组织.结果 43例结直肠癌组织中有25例(58.14%)Smad4 mRNA检测到阳性表达,其阳性表达率(58.14%)及表达水平(0.73±0.25)均低于相应的癌旁组织(88.37%,0.95±0.29)、腺瘤组织(90.63%,1.01±0.37)和健康人黏膜组织(100.00%,1.18±0.33),差异均有统计学意义(P＜0.05).Smad4基因启动子甲基化阳性率结直肠癌组织(60.53%)明显高于癌旁组织(27.03%)、腺瘤组织(25.00%)和健康人黏膜组织(16.67%),差异均有统计学意义(P＜0.05).Smad4蛋白表达的阳性率结直肠癌组织(44.19%)明显低于癌旁组织(81.40%)、腺瘤组织(87.50%)和健康人黏膜组织(91.67%),差异均有统计学意义(P＜0.05),并随着浸润深度加深和淋巴结转移,阳性率也随之下降.结论 Smad4的低表达与结直肠癌的发展、生物学行为和预后可能有关,可作为重要的生物学标志及病期评估的标志之一.     

趋化生长因子受体-7与结直肠癌淋巴管生成的关系第14期

目的 通过检测结直肠癌中趋化生长因子受体-7(CCR7)与血管内皮生长因子-D(VEGF-D)的表达,探讨二者的关系及临床意义.方法 应用免疫组化法检测124例结直肠患者和70例正常结肠黏膜中CCR7、VEGF-D和D2-40的表达.结果 CCR7和VEGF-D在结直肠癌中表达的阳性率明显高于正常结肠黏膜组织,D2-...     

BRG1在结直肠癌中的表达与预后和MMP-2的关系

目的分析结直肠癌组织中BRG1表达与结直肠癌临床病理特征及预后的关系,并初步探讨其机制.方法应用组织芯片及免疫组织化学方法检测1 1 2例结直肠癌组织和7 1例正常肠黏膜组织中BRG1及基质金属蛋白酶-2(matrix metalloproteinase-2,MMP-2)蛋白的表达,统计学分析BRG1表达与临床病理特征及患者预后的关系,并分析其与MMP-2表达的相关性.结果(1)B R G1和M M P-2在结直肠癌组织中的阳性率分别为66.1%和61.2%,较正常肠黏膜组织35.2%和3.3%明显增高(P0.01);(2)结直肠癌组织中BRG1高表达与结直肠癌患者临床病理特征包括患者性别、年龄、肿瘤大小、浸润深度、分化程度、淋巴结转移及临床分期之间均没有显著意义,但与患者5年总体生存率呈明显负相关,BRG1表达越高,患者预后越差;(3)结直肠癌组织中BRG1的表达与MMP-2呈正相关(r=0.307,P0.05).结论B R G1在结直肠癌组织中表达增高,可能成为结直肠癌患者的独立预后因子,原因可能与促进MMP-2异常表达有关.     

The cancer registry in cancer control

The sole justification for a cancer registry is that use is made of its data. The information stored and produced by a cancer registry forms the scientific basis for planning and organization of the treatment and prevention of cancer in the community. Its data can also be used in the testing of various hypotheses concerning the aetiology and biology of malignant neoplasms and it may also give rise to various new hypotheses.     

Causes of cancer and cancer prevention

Current understanding of the complex processes of cancer causation through a study of the mechanisms of carcinogenesis have documented that there are several major steps each, with distinct quantitative risk assessment factors. The first series of steps, defined by genotoxicity, deal with the assessment of the type of genotoxic carcinogen and its metabolism, leading to a DNA- and macromolecular-reactive species. A second area concerns the rate of cell duplication, important in leading to cell transformation to an early neoplastic state. The third key area explores agents that bear on a further development and growth of the transformed cells, an area that has quite distinct dose-response relationships from the first type. Therefore, modulation of the third area provides excellent means of control. In addition, of course, the optimal means is avoiding exposure to genotoxic carcinogens.     

Dendritic cell-based cancer immunotherapy for pancreatic cancer

Pancreatic cancer (PC) is a lethal disease and remains one of the most resistant cancers to traditional therapies. New therapeutic modalities are urgently needed, particularly immunotherapy, which has shown promise in numerous animal model studies. Dendritic cell (DC)-based immunotherapy has been used in clinical trials for various cancers, including PC, because DCs are the most potent antigen-presenting cell (APC), which are capable of priming naive T cells and stimulating memory T cells to generate antigen-specific responses. In this paper, we review the preclinical and clinical efforts towards the application of DCs for PC.     

Pancreatic cancer: progress in cancer therapy

Pancreatic cancer continues to be a highly lethal disease. In fact the overall 5-year survival rate is less than 4% and has hardly improved over the past two decades. Surgery is the only potential curative treatment, but the majority of patients have an unresectable disease at the diagnosis. After the demonstration in 1997 that gemcitabine could lead to an improvement in clinical benefit and overall survival this chemotherapy agent became the standard of care for advanced pancreatic cancer patients. Several authors tried to improve results obtained with single agent gemcitabine by exploring the activity of novel chemotherapy on biologically targeted agents in combination with gemcitabine. Unfortunately, global findings were often disappointing with only a marginally significant survival benefit. New treatment strategies and a more careful evaluation of innovative therapies are clearly needed for this disease. In this review we will focus on treatment strategies both in resectable and advanced pancreatic cancer.     

Dendritic cell-based cancer immunotherapy for colorectal cancer

Colorectal cancer(CRC) is one of the most common cancers and a leading cause of cancer-related mortality worldwide. Although systemic therapy is the standard care for patients with recurrent or metastatic CRC, the prognosis is extremely poor. The optimal sequence of therapy remains unknown. Therefore, alternative strategies, such as immunotherapy, are needed for patients with advanced CRC. This review summarizes evidence from dendritic cell-based cancer immunotherapy strategies that are currently in clinical trials. In addition, we discuss the possibility of antitumor immune responses through immunoinhibitory PD-1/PD-L1 pathway blockade in CRC patients.     

Colorectal cancer in hereditary breast cancer kindreds

PURPOSE: This study compared characteristics of colorectal cancer between families with dominant breast cancer inheritance and the general population. The cumulative incidence of colorectal cancer was also studied in genetically determined breast cancer syndrome subjects with BRCA1 and BRCA2 mutations and compared with the general population. METHODS: Subjects included 42 patients with colorectal cancer from 32 clinically determined hereditary breast cancer kindreds based on the autosomal dominant inheritance of breast cancers and early age of onset. The general population colorectal cancer cohort was composed of 755 patients from a tumor registry. Lifetime risk of colorectal cancer was determined in 164 BRCA1 and 88 BRCA2 gene mutation carriers and compared with the general population. Mean age of colorectal cancer onset, anatomic site distribution, histologic stage at presentation, and five year stage-stratified survival rates were compared between clinically determined hereditary breast cancer family members and the general population. RESULTS: The lifetime risk of colorectal cancer in male BRCA1 and BRCA2 mutation carriers was 5.6 percent, which was not different from 6 percent in males from the general population. Likewise, the lifetime colorectal cancer risk in female BRCA1 and BRCA2 mutation carriers was 3.2 percent, which was not different from 5.9 percent in females from the general population. Mean age of onset ± standard error for patients with colorectal cancer was 60±2 years for hereditary breast cancer kindreds compared with 67±0.4 years for the general population (P=0.0004). Colorectal cancer site distribution did not vary between hereditary breast cancer and the general population. Overall colorectal cancer stage distribution was significantly different, with more Stage I and fewer Stage IV cancers in subjects with hereditary breast cancer compared with the general population (P=0.01). Overall five year stage-stratified colorectal cancer survival rate ± standard error was 66±8 percent for hereditary breast cancer kindreds and 46±2 percent for the general population (P=0.023). CONCLUSION: Lifetime cumulative colorectal cancer incidence in subjects with BRCA1 and BRCA2 gene mutations was not different from the general population. However, significant differences in colorectal cancer were noted between hereditary breast cancer family members and the general population. Hereditary breast cancer-associated colorectal cancer had an earlier age of onset, lower tumor stage, and better survival rate than the general population. Except for age of onset, colorectal cancer in hereditary breast cancer kindreds exhibited more favorable characteristics than colorectal cancer in the general population.Read at the meeting of The American Society of Colon and Rectal Surgeons, San Antonio, Texas, May 2 to 7, 1998.     

糖尿病与胰腺癌、肝癌和结肠癌的关系及内在联系

糖尿病和糖耐量异常,切除胰腺癌后糖尿病改善,胰岛素需求量减少,对这类患者而言,糖尿病可以是胰腺癌的早期表现,因为胰腺癌与糖尿病的发生有明显的时间关联。这些患者多数年龄较大且无糖尿病家族史,体重指数在正常范围或有体重减轻,不肥胖,高血糖不稳定,需胰岛素治疗且很快发     

Familial history of cancer and lung cancer

There are many studies supporting the family history in lung cancer. In this study, we observed 1500 with lung cancer cases diagnosed between the years 1995-2000 in our clinic, and investigated family tendency of lung cancer in a control group including partners of 600 patients with family history of cancer. We conducted face-to-face interviews with 100 patients with lung cancer, and with first degree relatives of the other 1400 patients with lung cancer. There were 600 positive family history of cancer. Control populations were matches of the cancer patients with positive family history of cancer. Cases and controls were asked to report on their family history of cancer, as well as smoking status of family members. In conclusion, in 40% of 1500 patients with lung cancer, there was positive family history of lung cancer with regard to malignity. This positive family history of cancer was consisted of 51.8% lung cancer, 35.5% digestive cancer and 12.7% other cancers such as breast, larynx, prostate and bone. In control group, the value of the positive family history of lung cancer with regard to malignity was 5.0% (p< 0.001). These results support the hypothesis of a genetic susceptibility by showing that the patients with lung cancer have significantly more positive family history of lung cancer and digestive cancer.     

The cancer registry in cancer control--a review

The author reviews key elements in the contribution of the cancer registry to cancer control. A cancer registry always requires the direct or indirect cooperation of the medical profession in the reporting of new cancer cases and it must in return provide services which the physician can use in the care of cancer patients. Survival of patients can be assessed and treatment evaluated for the entire reporting area and not just for selected groups. Projections of the needs for future material and manpower resources can be made on the basis of data collected by the registry. The cancer registry is also in an ideal position to monitor the efficacy of screening programs. Data collected by the registry are the basis for epidemiologic investigations. The magnitude of the cancer problem can be measured and variation by time and place identified. The origin of cancer can be studied by a variety of epidemiologic approaches using data from the cancer registry. Should a suspected etiologic factor be altered in the environment the impact of the intervention may be followed using trend data from the registry. The linkage if individual records is essential if the registry is to function accurately and efficiently. Appropriate safeguards for the confidentiality of medical data must be insured. Adequate staffing with persons interested in and able to undertake the analysis and interpretation of the data collected is a must if the cancer registry is to live up to its potential.