小鼠一体多瘤模型复制与S180脉冲致敏树突状细胞抗瘤特异性观察

目的 :复制一种新的荷瘤动物模型 ,同一小鼠皮下 ,不同部位荷 3种不同类型肿瘤 (S180、H2 2、EAC瘤株 ) ,继之以一种肿瘤抗原 (冻融S180细胞 )脉冲刺激的树突状细胞 (DC)免疫治疗 ,观察其效应。方法 :昆明小鼠随机分为 5组 ,6只 /组 ,1、2、3组分别荷单一瘤株S180、H2 2和EAC瘤细胞 ;4、5组荷以上 3种瘤株 ;所接种的 3种瘤细胞数均为 6× 10 6,接种部位二侧后腿腋下和背部 ,分别交替接种 3种瘤细胞株 ,其中每 2只接种部位相同 ,第 5组另接受肿瘤抗原 (冻融S180细胞 )脉冲刺激DC行免疫治疗。观察接种后瘤体大小和特异的淋巴细胞毒杀伤活性(CTL)。结果 :1～ 4组组间相比 ,单一荷瘤与复合荷瘤的相同瘤株在肿瘤生长速度上基本相同 (P >0 .0 5 ) ,4组荷瘤鼠生存期相近 (P >0 .0 5 )。与 1～ 4组荷同一瘤株鼠比较 ,脉冲DC免疫治疗鼠 (第 5组 ) ,S180、H2 2和EAC瘤株的增生速度明显减缓 ,荷瘤第 3周时 ,S180、H2 2增生减缓更为明显 (P <0 .0 1) ;EAC瘤株亦呈同样变化趋势 ,但幅度较小。CTL结果显示 ,T淋巴细胞对S180和H2 2瘤细胞株均有很强杀伤活性 (78% ,72 % ) ,而对EAC瘤株杀伤活性较弱 (34% )。结论 :同一小鼠体内同时荷 3种移植瘤株即一体多瘤动物模型可行 ;S180致敏的DC介导T细胞既可杀灭S180又可杀灭H2     

流式细胞术检测肿瘤患者红细胞CD35表达与红细胞黏附功能相关性研究

目的 探讨红细胞CD35表达数量与红细胞免疫黏附肿瘤细胞活性相关性,研究恶性肿瘤患者红细胞CD35表达数量及免疫黏附功能的变化规律.方法 选择原发性肺癌40例,胃癌32例,结肠癌36例及40例健康人血标本,用流式细胞术（FCM）检测红细胞CD35几何平均荧光强度（CMFI）;EAC花环试验检测红细胞免疫黏附肿瘤细胞花环率.结果 肺癌、胃癌、结肠癌组较正常对照组红细胞黏附肝癌细胞BEL-7402花环率下降,t值分别为3.069、3.429、3.056,P值分别为0.004,0.002、0.004,差异有统计学意义（P＜0.01）;肺癌、胃癌、结肠癌组间花环率比较,F=0.844,P=0.433,差异无统计学意义（P＞0.05）.肺癌、胃癌、结肠癌组较正常对照组红细胞CD35 GMFI降低,t值分别为3.392、2.767、3.635,P值分别为0.002、0.009、0.001,差异有统计学意义（P＜0.01）;肺癌、胃癌、结肠癌组间红细胞CD35 GMFI比较,F=0.717,P=0.491,差异无统计学意义（P＞0.05）.肺癌、胃癌、结肠癌、正常对照组红细胞黏附肿瘤花环率与其红细胞CD35 GMFI呈正相关,相关系数分别为0.628、0.859、0.636、0.887,P值分别为0,000、0.000、0.000、0.000,有统计学意义（P＜0.01）.结论 肺癌、胃癌、结肠癌组红细胞黏附功能下降;肺癌、胃癌、结肠癌组红细胞CD35表达降低;肺癌、胃癌、结肠癌、正常对照组红细胞黏附肿瘤花环率与其细胞CD35 GMFI呈正相关;流式细胞术（FCM）检测红细胞CD35的表达是一种准确、快速、高效的肿瘤患者红细胞免疫功能检测方法.     

Antiproliferative and hepatoprotective activity of metabolites from Corynebacterium xerosis against Ehrlich Ascites Carcinoma cells

ObjectiveTo find out the effective anticancer drugs from bacterial products, petroleum ether extract of Corynebacterium xerosis.MethodsAntiproliferative activity of the metabolite has been measured by monitoring the parameters like tumor weight measurement, tumor cell growth inhibition in mice and survival time of tumor bearing mice, etc. Hepatoprotective effect of the metabolites was determined by observing biochemical, hematological parameters.ResultsIt has been found that the petroleum ether extract bacterial metabolite significantly decrease cell growth (78.58%; P<0.01), tumor weight (36.04 %; P<0.01) and increase the life span of tumor bearing mice (69.23%; P<0.01) at dose 100 mg/kg (i.p.) in comparison to those of untreated Ehrlich ascites carcinoma (EAC) bearing mice. The metabolite also alters the depleted hematological parameters like red blood cell, white blood cell, hemoglobin (Hb%), etc. towards normal in tumor bearing mice. Metabolite show no adverse effect on liver functions regarding blood glucose, serum alkaline phosphatases, glutamic pyruvic transaminase, glutamic oxaloacetic transaminase activity and serum billirubin, etc. in normal mice. Histopathological observation of these mice organ does not show any toxic effect on cellular structure. But in the case of EAC bearing untreated mice these hematological and biochemical parameters deteriorate extremely with time whereas petroleum ether extract bacterial metabolite receiving EAC bearing mice nullified the toxicity induced by EAC cells.ConclusionStudy results reveal that metabolite possesses significant antiproliferative and hepatoprotective effect against EAC cells.     

Pembrolizumab for the treatment of esophageal cancer

ABSTRACT

Introduction

Esophageal cancer (EC) is the seventh most common cancer and the sixth leading cause of cancer death. However, the prognosis of unresectable advanced or recurrent EC patients remains poor and there are few effective therapeutic agents for EC. Pembrolizumab is a monoclonal antibody that exerts anti-tumor activity by inhibiting the interaction of programmed cell death protein 1 with its ligand (PD-L1) on activated lymphocytes. Pembrolizumab monotherapy shows a significant survival benefit in metastatic or recurrent EC patients with PD-L1 CPS ≥10 as second-line treatment.     

Efficacy and safety outcomes of multimodal endoscopic eradication therapy in Barrett’s esophagus-related neoplasia: a systematic review and pooled analysis

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Current state of prognostication,therapy and prospective innovations for Barrett’s-related esophageal adenocarcinoma: a literature review

ObjectiveBarrett’s esophagus (BE) is the only known precursor to esophageal adenocarcinoma (EAC), which has one of the lowest 5-year survival rates in oncology. The reasons for poor survival are twofold: the large majority of diagnoses are in advanced stages (~80%) and limited treatment options, with a deficit of biology-guided therapies. As a rapidly growing public health concern with poor prognosis, research into the molecular progression for BE and novel therapeutics for EAC currently has high clinical utility. Review of the literature reveals that innovative analysis of metaplastic progression from BE to EAC at a molecular level can shed light on the underlying transformative probabilities of BE into malignant pathologies and may impact current of future therapeutic modalities for management of these diseases.BackgroundEAC is the fastest increasing cancer in the United States with a 600% increase over the past 25 years. This cancer arises from dysplastic tissue of BE, a complication of gastroesophageal reflux disease (GERD). Chronic acid and bile reflux in the distal esophagus initiates a metaplastic conversion of normal squamous epithelium to premalignant intestinalized columnar epithelium. Patients with BE have a 125-fold higher risk of cancer compared to the general population.MethodsWe critically reviewed the current status of BE monitoring, and subsequent therapeutic strategies being used in patients who have progressed to cancer. Also, new diagnostic tools and therapeutic candidates for BE-related EAC are discussed. Highly-targeted searches of databases containing recent original peer-reviewed papers were utilized for this review.ConclusionsNovel and well-described biomarkers analyzed in the patient’s diseased tissue will provide for more powerful diagnostics, but also possess the potential to develop strategies for personalized management and identify targets for intervention to either cease disease progression or treat BE and/or EAC. Since millions of Americans develop BE without progressing to cancer, there is a critical need to identify the small percentage of Barrett’s patients who possess hallmarks of disease progression or carcinogenesis with novel screening techniques. Incorporation of such tools into standard screening protocols for BE surveillance and/or therapy would be critical to detect malignant transformations before clinically obvious cancer ever develops.