首页 > 文献资料
-
乙肝病毒诱导原发性肝细胞癌发病机制研究的进展
大量流行病学资料表明,原发性肝细胞癌(primary hepatocellular carcinoma,PHC)的发病率和HBsAg阳性率具有明显的地理分布相关性.同时还显示:乙型肝炎病毒(hepatitis B virus,HBV)感染人群中发生肝癌的相对危险度为非感染人群的100倍以上.
-
超声造影诊断肝硬化合并肝细胞性肝癌一例
患者男性,44岁.24年前查体发现乙肝表面抗原阳性,无其他不适,2周前偶感右上腹隐痛不适,无黄疸、乏力、食欲减退、皮肤瘙痒、齿龈出血等表现,4天前于外院复查超声发现"右肝后叶门静脉支栓塞",遂行进一步检查.
-
Objective To study the effect of spleen lymphocytes on the splenomegaly by hepatocellular carcinoma-bearing mouse model.
Methods Cell counts, cell cycle distribution, the percentage of lymphocytes subsets and the levels of IL-2 were measured, and two-dimensional gel electrophoresis (2-DE) was used to investigate the relationship between spleen lymphocytes and splenomegaly in hepatocellular carcinoma-bearing mice.
Results Compared with the normal group, the thymus was obviously atrophied and the spleen was significantly enlarged in the tumor-bearing group. Correlation study showed that the number of whole spleen cells was positively correlated with the splenic index. The cell diameter and cell-cycle phase distribution of splenocytes in the tumor-bearing group showed no significant difference compared to the normal group. The percentage of CD3+ T lymphocytes and CD8+ T lymphocytes in spleen and peripheral blood of tumor-bearing mice were substantially higher than that in the normal mice. Meanwhile, the IL-2 level was also higher in the tumor-bearing group than in the normal group. Furthermore, two dysregulated protein, β-actin and S100-A9 were identified in spleen lymphocytes from H22-bearing mice, which were closely related to cellular motility.
Conclusion It is suggested that dysregulated β-actin and S100-A9 can result in recirculating T lymphocytes trapped in the spleen, which may explain the underlying cause of splenomegaly in H22-bearing mice. -
PTEN在肝癌组织中的表达及其与肿瘤细胞凋亡的关系
PTEN是一种抑癌基因,我们通过检测肝细胞肝癌(HCC)组织中PTEN蛋白的表达及肿瘤细胞的凋亡情况,探讨其临床意义.
-
Objective: To achieve an optimized method for soluble expression of human carboxylesterase 1 (hCE-1) in escherichia coil and purification by Ni2+-NTA agarose affinity chromatography, to get improved protein yield and purity for further development of hepatocellular carcinoma (HCC) diagnosis ELISA kits. Methods: The best antigen epitopes of hCE1 were predicted by comparing secondary structure, flexible regions, hydrophilicity, antigenic index surface probability of residues. Afterwards, pET-42a (+) with a His-tag and a GST-tag was applied to form recombinant plasmid pET-42a (+)/hCE1, which facilitated purification when using Ni2+-NTA agarose affinity chromatography. Protein quality was measured by SDS-PAGE and BCA protein assay. Western-blot identification was also performed to ensure the correct expression of hCE1 protein. Results: The residues from 500 to 567 near C-terminal of hCE1 protein were considered the best epitopes which exhibited high hydrophilicity and high surface probability and relatively flexible secondary structure and low homology compared with hCE2 and hCE3. His-hCE1 500-567 fusion protein was achieved by IPTG-inducted expression with an expected mass of 42 kDa. After purification, the final product was specially identified, which reached over 95%purity and more than 10 mg/L of microbial culture. In Western blot, the purified fusion protein was recognized by anti-hCE1 monoclonal antibody, along with previous sequencing validation, which demonstrated the correct preparation of soluble hCE1 protein. Conclusion: This is an efficacious and affordable strategy to generate fusion hCE1 of high quality in E coli, which facilitates preparation of hCE1 monoclonal antibody and further HCC diagnosis research.
-
肝癌治疗新药临床研究进展
90%的肝癌为肝细胞癌(hepatocellular carcinoma,HCC),是全球除胃癌和食管癌外的第3种常见肿瘤,全世界每年新增肝癌病例超过100万.我国是全球肝癌发病率高的国家,在常见肿瘤中肝癌发病率仅次于肺癌,居第2位.肝癌恶性程度较高、病情进展快,大部分患者(>50%)就诊时己为晚期,不适合手术切除.即便可以手术切除的肝癌,2年复发率也高达50%.晚期肝癌的治疗相当棘手,尚无标准治疗方案,预后差,传统化疗后平均中位生存期仅为3~5个月.过去的20年间,肝癌患者的相对5年生存率仅由3%增长到4%~7%~[1],主要原因归结于肝癌的高复发性和没有有效的药物治疗.肝癌的药物治疗可归纳为
-
脾窦岸细胞血管瘤合并慢性乙型肝炎及原发性肝细胞癌一例
患者男,50岁.因上腹部胀痛不适1周于2006年12月入院.患者有乙型肝炎病史15年,未曾治疗.体检:腹稍隆,无明显压痛及反跳痛,肝脾肋下未扪及,肝区及双肾区无扣痛.
-
乙型肝炎病毒X基因与肝细胞癌
当前发现乙型肝炎病毒(HBV)基因组中的X基因及其编码产物X蛋白(hepatitis B virus X protein,HBx)是HBV中惟一具有多种调控功能的病毒蛋白质.
-
肝癌前病变与高分化肝癌的病理诊断与鉴别
病毒性肝炎、肝硬化是肝细胞癌发生的主要病理基础.大多数的肝癌患者均伴有肝硬化.从肝炎、肝硬化到肝癌,其形态改变往往是连续的,即:肝炎-肝硬化-巨大再生性结节-腺瘤性增生-不典型腺瘤性增生-高分化肝癌(或称早期肝癌)-进展期肝癌.对多数病理医生来说,肝炎、肝硬化以及进展期肝癌由于细胞形态良恶性明显而比较容易诊断.而形态介于其间的腺瘤性增生、不典型腺瘤性增生与高分化肝癌之间的鉴别则非常困难.我们认为对此类病例必须从理论上熟悉其特点,在实际工作中熟悉其病变,尽量使用统一的诊断标准.在此综合结合自己的粗浅体会,对此问题作一总结.
-
丙型肝炎病毒感染相关肝癌的宿主易感基因研究进展
丙型肝炎病毒( HCV)感染是引发肝细胞肝癌( HCC)的重要危险因素,病毒与宿主的相互作用在肝癌的发生机制中起重要作用。宿主易感基因的检测有助于肝癌的个体化防治及改善预后。本文就HCV感染相关肝癌的宿主易感基因的研究进展进行综述。
-
Objective: To investigate the expression levels of total and phosphorylation p38 , JNK and ERK1/2 protein during diethylnitrosamine ( DEN)-induced rat hepatocellular carcinoma occurrence and develop-ment. Methods: To induce hepatocellular carcinoma, we performed intermittently administrated DEN to rats. Using light microscopy and electron microscopy technique to discover that liver tissue morphological changes in the process. And then the expression of p38, JNK, ERK1/2 mRNA and protein was performed by RT-PCR and west-ern blot analysis, in order to furthermore explore the association of them. Results:In rat hepatoma model develop-ment, protein of p-p38、p-ERKl/2、p-JNK and its mRNA expression were significantly increased with increasing treatment time, but,no significant changes of p38, ERK, of JNK protein and its mRNA expression. Conclusions:During DEN-induced rat hepatocellular carcinoma, p-p38 and p-ERK proteins expressed lower and p-JNK pro-tein expressed high, and its expression was positively correlated with the development of hepatocellular carcinoma.
-
AFP及GP73的联合检测与肝细胞癌早期诊断和复发监测
IntroductionHepatocellular carcinoma ( HCC) is one of the most prevalent malignancies worldwide,with an increasing incidence in the United States and Europe, and the third most common cause of cancer-related death worldwide[1-2] .Based on the GLOBOCAN 2008 estimates, about 748 300 new liver cancer cases and 695 900 cancer deaths occurred worldwide in 2008 ,collected and made available by the World Health Organization ( WHO) [3].
-
超声造影在肝硬化增生结节及小肝癌鉴别诊断中的研究进展
肝细胞肝癌是世界上第六大常见恶性肿瘤,占癌症死亡原因的第三位[1],原发性肝癌是肝硬化严重的并发症之一,小肝癌(small hepatocellular carcinoma,SHCC)的早期诊断是提高肝癌患者生存率的关键因素.穿刺活检病理学检查仍被视为诊断的金标准,但由于其有创性不易被患者接受,且对于位置深的小病灶假阴性率也较高.二维超声检查因其无创及可重复等优点常作为肝硬化及肝癌的诊断及随访方法.
-
肝癌转移复发的临床蛋白质组学研究现状及进展
肝细胞性肝癌(HCC)是一种多基因参与、多因素、病理机制复杂的常见恶性肿瘤.该病多发于非洲、中国和东南亚地区,全世界每年约50~100万人死于肝癌.
-
肝细胞癌的病因及化学预防
肝细胞癌是世界上常见的恶性肿瘤之一.即使是在外科切除这样的根治疗法之后,其复发率还极高.肝炎病毒,黄曲霉毒素,酒精,饮水污染和遗传因素是其主要病因.能通过化学预防限制这种趋势吗?癌的化学预防,可定义为用特定的天然或合成的化学制剂去倒转、抑制阻止侵袭性的癌的发生,作为一种癌控制的新方法而获得显著成效.现综述维甲酸类、干扰素、奥替普拉、环氧合酶2抑制剂、硒、姜黄素及叶绿酸在肝细胞癌化学预防中的作用.化学预防是肿瘤学中出现的一个新领域,在这个领域基础和临床的研究者都面临极大的挑战.
-
卵圆细胞及其与原发性肝癌关系的研究进展
尽年来,有关干细胞的研究已经得到广泛的注意,肝卵圆细胞(HOC)被认为是肝脏干细胞的子代,是肝脏干细胞到成熟肝细胞的中间体,他既可以向胆管细胞分化,又可向肝细胞分化.目前认为肝卵圆细胞分为三型,Ⅰ型细胞体积较小,核大,胞质少,此为原始的卵圆细胞.Ⅱ型细胞体积稍大,胞质稍多,此为向胆管上皮分化的胆管样卵圆细胞.Ⅲ型细胞体积稍大,内含稍多粗面内质网,此为向肝细胞分化的肝细胞样卵圆细胞.肝卵圆细胞定位于赫氏小管区(Hering管)和胆管树终末处,与骨髓干细胞有大量共同的表面标志,受多种细胞因子的调控,已经在体外分离培养成功,并发现存在于肝癌组织中.肝卵圆细胞"成熟受阻"可能是导致原发性肝癌的原因之一,其向原发性肝癌转化的机制仍不清楚,可能是多个癌基因和/或抑癌基因共同调控的结果.本文就此研究进展作一综述.
-
三氧化二砷治疗肝癌的分子机制
三氧化二砷(As2O3)在白血病和各类实体瘤的治疗中广泛应用.肝细胞肝癌(hepatoceuular carcinoma,HCC)是消化系统常见的肿瘤.其恶性程度高、预后差.As2O3在与肝癌细胞的研究表明,他可以发挥细胞凋亡的正向调控作用,抑制肿瘤细胞增殖,是较好的抗肿瘤药物之一.但As2O3同时作为一种致癌物,与含巯基的大分子蛋白结合,影响细胞的正常代谢,导致细胞内信号转导通路异常调节,抑癌基因失活等,从而引起皮肤异常改变和其他内脏肿瘤如肝癌、肺癌、膀胱癌的发生.因此研究As2O3对肝细胞作用的机制对有效防治HCC有很重要的意义.本文从As2O3的生物学抗癌效应入手综述其治疗肝癌的分子机制.
-
生长抑素类似物治疗肝细胞肝癌的抗肿瘤作用及其机制
人工合成的生长抑素类似物血浆半衰期长,作用更强大,耐受性良好,新研究表明,对多种实体肿瘤亦有抑制作用.本文就生长抑素类似物对肝细胞肝癌的抗肿瘤作用及其机制方面的国内外研究进行综合阐述,从其各种化学结构、作用受体亚型、以及肝脏肿瘤受体表达,进而证实了生长抑素类似物对肝脏肿瘤的治疗作用,具体包括原发性肝癌、转移性肝癌、原位种植瘤等.同时研究表明生长抑素类似物抗肿瘤作用机制可能包括两大方面:直接及间接作用,前者通过特异性受体发挥作用;后者通过抑制促肿瘤生长的激素及细胞因子的分泌,或抑制肿瘤血管形成,或调节机体免疫活性,或诱导肿瘤细胞发生凋亡等间接阻止肿瘤生长.进一步阐明其抗肿瘤机制将有可能在肝肿瘤治疗方面开辟出一条新的途径,并产生广阔的临床应用前景.
-
热休克蛋白家族与肝癌的关系
热休克蛋白HSP是一种广泛存在于微生物和动植物体内的一种应激蛋白.HSP在HCC的生物治疗中将发挥越来越重要的作用.HSP在生物体内起着参与加速降解和清除细胞代谢产物,维护细胞的功能和生存,协同免疫应答,调节信号传导通路,调控细胞周期,抑制凋亡以及促进微管的形成与修复等作用.大量研究显示一些HSP在肿瘤免疫中发挥作用,并有望制成基因疫苗应用于肿瘤的防治.本文综述了HSP70,HSP90,HSP47,HSP27等在肝癌的发生、发展和治疗中的进展及其在肝癌防治中的意义.
-
乙型肝炎病毒慢性感染和肝癌发生
0引言肝细胞癌(hepatocellular carcinoma,HCC)是人类常见的恶性肿瘤之一.在世界范围内居男性常见恶性肿瘤的第7位,居女性第9位;在中国被列为男性恶性肿瘤的第3位,仅次于胃癌和食管癌.全世界每年大约43.7万人被诊断为HCC,其中约一半发生在中国.多数HCC在发现时已进入进展期,恶性程度高,其5 a存活率小于3%[1].近年来的流行病学和实验室研究初步表明,HCC的主要发病因素有乙型肝炎病毒(hepatitis Bvirus,HBV)或丙型肝炎病毒(hepatitis C virus,HCV)慢性感染、黄曲霉素B1(aflatoxin B1,AFB1)的摄入以及酗酒.在我国,HBV慢性感染是一种常见的致病因素,在启东和广西的某些地区还有AFB1摄入这一因素同时存在.