分化相关基因NDRG1在恶性肿瘤中的研究进展

恶性肿瘤是危害人类健康的重要疾病之一,其发生发展是一个多因素作用、多基因参与、经过多个阶段才最终形成的极其复杂的生物学现象。随着人癌基因和抑癌基因的发现,人们已认识到恶性肿瘤是一种基因分子疾病。近年来,恶性肿瘤发病率逐年升高,发病年龄年轻化,在全球范围内,其防治仍是当今生命科学研究领域的一个难点。因此,如果能找出有预警作用的标志物,在癌变早期准确预报;找到促进肿瘤细胞分化,逆转其恶性表型,减少其侵袭转移的基因,肿瘤的防治就会有战略性突破。NDRG1基因是近年来新发现的一种分化相关基因,本文以NDRGI基因在恶性肿瘤发生发展过程中的作用为基础,对该基因的结构、功能和作用机制进等行如下综述：     

分化相关基因NDRG1在恶性肿瘤中的研究进展

恶性肿瘤是危害人类健康的重要疾病之一,其发生发展是一个多因素作用、多基因参与、经过多个阶段才最终形成的极其复杂的生物学现象.随着人癌基因和抑癌基因的发现,人们已认识到恶性肿瘤是一种基因分子疾病.近年来,恶性肿瘤发病率逐年升高,发病年龄年轻化,在全球范围内,其防治仍是当今生命科学研究领域的一个难点.因此,如果能找出有预警作用的标志物,在癌变早期准确预报;找到促进肿瘤细胞分化,逆转其恶性表型,减少其侵袭转移的基因,肿瘤的防治就会有战略性突破.     

RCAN1在恶性肿瘤中的研究进展

钙调神经磷酸酶调节蛋白(Regulator of calcineurin 1,RCAN1)作为与钙调神经磷酸酶(Calcineurin,CaN)发生相互作用的内源性蛋白,在许多恶性肿瘤细胞中广泛表达,如小细胞肺癌、甲状腺癌、白血病、肝癌、恶性胶质细胞瘤、子宫内膜腺癌等。近年来研究显示,当RCAN1呈高表达状态时,可以通过多种途径来抑制肿瘤的增殖、分化、侵袭和转移,从而抑制肿瘤的进展。这些研究结果对患者的生存期和预后评估有着重要的指导作用,并对恶性肿瘤的治疗和干预奠定了一定的理论基础。     

HMGB1在消化系统恶性肿瘤中的研究进展

摘 要：消化系统恶性肿瘤在我国恶性肿瘤中较常见,有较高的发病率和死亡率,其早期诊断率低,预后较差。高迁移率族蛋白（HMGB1）是一种非组蛋白染色体结合蛋白,主要存在于细胞核中。近年来研究显示,消化系统肿瘤如肝癌、胃癌、结直肠癌、胰腺癌、食管癌等恶性肿瘤中HMGB1过量表达。当外界环境发生改变时,HMGB1可以主动或被动释放至细胞外,引起下游信号通路的激活,促使肿瘤细胞发生转移、浸润。HMGB1有望成为消化系统恶性肿瘤治疗的新靶点。全文就HMGB1在消化系统恶性肿瘤中的研究进展作一综述。     

LRIG1在恶性肿瘤中的研究进展

LRIG是新发现的一种基因,其家族成员包括LRIG1、LRIG2和LRIG3。目前研究较多的是LRIG1,且研究证实在人体正常组织内广泛表达而在大部分肿瘤中表达下调或缺失,提示其可能作为一种抑癌基因,调控肿瘤细胞的生长、增殖、侵袭、转移[1]。现就近几年LRIG1与几种恶性肿瘤之间的研究予以综述。1 LRIG1的结构LRIG1的小鼠同源基因是Lrig1,该基因定位于人染色体     

RB1在恶性肿瘤中的研究进展

视网膜母细胞瘤基因1(Retinoblastoma1,RB1)是人类发现的第一个抑癌基因,因为最初在视网膜母细胞瘤中发现该基因所以命名为视网膜母细胞瘤基因1. RB1作为一种负性调控因子在细胞周期中有重要作用,通过与转录因子E2 F结合来调控细胞的增殖. 研究还发现RB1在抗细胞凋亡中也扮演着重要的角色,RB1的敲除可以增强抗肿瘤药物导致细胞死亡的敏感性. RB1的这种双重作用提示其可能是恶性肿瘤的发病原因,并且可能成为肿瘤进展及临床治疗效果的预测指标.     

转移抑制基因KAI1在妇科恶性肿瘤中的研究进展

癌细胞侵袭转移是影响癌症患者疗效和导致预后差的主要原因,其机制复杂。它包括肿瘤细胞脱离原发灶,侵袭黏附于细胞外基质,同时分泌蛋白水解酶,降解基质,进入血管和淋巴管,通过黏附于内皮细胞在适宜部位驻留,诱导血管生成,逃避机体免疫系统的攻击,在远隔部位形成转移灶。整个过     

微粒体谷胱甘肽S-转移酶1在恶性肿瘤中的研究进展

微粒体谷胱甘肽S-转移酶1(microsomal glutathione S-transferase 1,MGST1)是谷胱甘肽S-转移酶(glutathione S-transferase, GST)超家族和花生四烯酸与谷胱甘肽代谢中的膜相关蛋白(membrane-associated proteins in eicosanoid and glutathione metabolism, MAPEG)超家族的共同成员,它通过催化外源性物质的II相解毒过程,从而保护细胞膜免受氧化应激的损伤。众多研究发现MGST1与恶性肿瘤的发生发展密切相关,有望成为癌症治疗的新型分子靶点。本文就MGST1在恶性肿瘤中的研究进展予以综述。     

血清C4,C5测定在恶性肿瘤疾病中的意义

本文通过血清中 C_4、C_5的测定,对几种恶性肿瘤进行了探讨,共测定了77例,其中肺癌53例(小细胞肺癌5例);乳腺癌18例;食道癌6例;健康献血员作为正常对照组测定30例;并做了20例良性疾病的测定。材料和方法一、标本来源:检材取自住院及门诊已确定诊断而又未进行治疗的恶性肿瘤患者,采血后立即分离血存-20℃低温冰箱中待检。二、试验步骤:1、试剂:有单价特异的 C_4及 C_5抗血清、参考标准血清购自上海生物制品所。需要配制pH8.6的巴比妥缓冲液,并准备优质的琼脂或琼脂糖。2、方法:用巴比妥缓冲液稀释 C_4或C_5抗血清,稀释倍数分别为抗血清瓶签上所示     

Update on the role of C1GALT1 in cancer

Cancer remains one of the most difficult diseases to treat. In the quest for early diagnoses to improve patient survival and prognosis, targeted therapies have become a hot research topic in recent years. Glycosylation is the most common posttranslational modification in mammalian cells. Core 1β1,3-galactosyltransferase (C1GALT1) is a key glycosyltransferase in the glycosylation process and is the key enzyme in the formation of the core 1 structure on which most complex and branched O-glycans are formed. A recent study reported that C1GALT1 was aberrantly expressed in tumors. In cancer cells, C1GALT1 is regulated by different factors. In the present review, the expression of C1GALT1 in different tumors and its possible molecular mechanisms of action are described and the role of C1GALT1 in cancer development is discussed.     

C1GALT1 in health and disease

O-linked glycosylation (O-glycosylation) and N-linked glycosylation (N-glycosylation) are the two most important forms of protein glycosylation, which is an important post-translational modification. The regulation of protein function involves numerous mechanisms, among which protein glycosylation is one of the most important. Core 1 synthase glycoprotein-N-acetylgalactosamine 3-β-galactosyltransferase 1 (C1GALT1) serves an important role in the regulation of O-glycosylation and is an essential enzyme for synthesizing the core 1 structure of mucin-type O-glycans. Furthermore, C1GALT1 serves a vital role in a number of biological functions, such as angiogenesis, platelet production and kidney development. Impaired C1GALT1 expression activity has been associated with different types of human diseases, including inflammatory or immune-mediated diseases, and cancer. O-glycosylation exists in normal tissues, as well as in tumor tissues. Previous studies have revealed that changes in the level of glycosyltransferase in different types of cancer may be used as potential therapeutic targets. Currently, numerous studies have reported the dual role of C1GALT1 in tumors (carcinogenesis and cancer suppression). The present review reports the role of C1GALT1 in normal development and human diseases. Since the mechanism and regulation of C1GALT1 and O-glycosylation remain elusive, further studies are required to elucidate their effects on development and disease.     

FLOT-1在人类实体肿瘤中的研究进展

浮舰蛋白-1（flotillin-1,FLOT-1）属于脂筏标记蛋白,参与多种细胞生理活动,与许多肿瘤发生发展密切相关。FLOT-1在乳腺癌、食管鳞状癌、肾细胞癌（renal cell carcinoma,RCC）、移行细胞癌（transitional cell carcinoma,TCC）、非小细胞肺癌（nonsmall cell lung cancer,NSCLC）、肝细胞癌等肿瘤中均高表达,并与临床分期、转移、浸润和预后相关。本文综述了FLOT-1的结构和功能,及其在多种人类实体肿瘤中的作用。      

Fibronectin in human solid tumors

Fibronectin in human solid tumors was studied by indirect immunofluorescence staining of biopsy material. Altogether 73 tumors were examined, comprising 12 sarcomas, 3 melanomas I reticulum cell sarcoma, 39 carcinomas, 6 benign soft-tissue tumors and 12 benign epithelial tumors. In all sarcomas the individual tumor cells were surrounded by a network of fibronectin which was continuous with the stroma. The distribution of fibronectin was similar in the benign soft-tissue tumors. In contrast, no fibronectin was detected in the individual carcinoma cells or in their periphery. However, the reactive connective tissue stroma of carcinomas was strongly positive for fibronectin. This was true also for the stroma of benign epithelial tumors. These results show that, contrary to the situation in cell culture, in vivo sarcoma cells and benign soft-tissue tumor cells contain fibronectin in their pericellular matrix. On the other hand, fibronectin can be used to distinguish carcinomas from sarcomas in vivo.     

贝伐单抗在部分实体肿瘤中临床应用的研究进展

随着临床研究的深入,抗血管内皮生长因子(vascular endothelial growth factor,VEGF)抗体的靶向治疗越来越受到重视,其中贝伐单抗(bevacizumab,BV)成为关注的焦点,并于今年2010年5月在中国成功上市。本文就BV在转移性结直肠癌(metastatic colorectal cancer,mCRC)、非小细胞肺癌(non-small cell lung cancer,NSCLC)、转移性乳腺癌(metastatic breast cancer,mBC)及转移性肾细胞癌(metastatic renal cell carcinoma,mRCC)的靶向治疗中的研究进展作一综述。     

PD-1/PD-L1在实体肿瘤组织中表达的研究进展

程序性死亡受体配体1（programmed death ligand 1,PD-L1）是一种参与免疫抑制通路的分子,在较多实体肿瘤细胞及其周围T淋巴细胞表面显著表达,能够与其受体程序性死亡受体1（programmed death-1,PD-1）结合,抑制肿瘤组织周围的免疫微环境,促使肿瘤细胞逃避免疫监视作用。本文就PD-1/PD-L1在不同实体肿瘤组织中表达的研究进展作一综述。     

Proto-oncogenes activation in human solid tumors

Genetic alterations in solid human tumors occur in several groups of genes, one of which contains the proto-oncogenes. These genes are involved in the control of cell proliferation and become activated in oncogenes by various mechanisms. These activations are reviewed herein.     

The role of Notch signaling in human cervical cancer: implications for solid tumors

The detection of intracellular forms of Notch1 in human cervical cancers more than a decade ago prompted an investigation into the possible role of this pathway in driving these cancers. These tumors are consistently characterized by features of deregulated ligand-dependent signaling. Although Notch signaling complements the function of papillomavirus oncogenes in transformation assays of human keratinocytes, there are dose-dependent effects, which inhibit growth of established cervical cancer cell lines. Two pro-oncogenic effector mechanisms that have been suggested to operate in this context by Notch signaling are the activation of PI3K/Akt pathway and the upregulation of c-Myc. Collectively, there is a complex interplay between Notch signaling and papillomaviruses in the context of cervical carcinogenesis. Better animal model systems and identification of human cervical cancer stem cells should help clarify the possible stage specific and pleiotropic effects and regulation of Notch signaling.     

Natural killer cells in human solid tumors

Natural killer (NK) cells have been studied in human neoplastic diseases in an effort to assess the role of these cells in the control of human neoplasia and to monitor the effects of therapeutic regimens expected to affect this reactivity. NK activity measured against susceptible cell lines is usually somewhat depressed in patients bearing advanced solid tumors, but not at early disease stages. Lymphoid cells associated with solid tumor tissues or effusions have usually low NK cytotoxicity, with considerable differences among histologic types (e.g., nasopharyngeal carcinoma versus other tumors) or at different sites involved by the same tumor (e.g., peritoneal effusions versus solid lesions in ovarian carcinoma). The low levels of NK activity of tumor-associated lymphoid cells are primarily related to a low frequency in the relevant effector cells at the tumor site, although suppression of the in vitro maintenance of cytotoxicity by in situ macrophages and lymphocytes has been described in a few patients. Treatment with immunopharmacologic agents, interferons in particular, has been reported to augment NK activity in cancer patients, but it is unclear how blood NK activity relates to tissue levels of this reactivity. Limited evidence indicates that blood NK levels need not be representative of the activity of tumor associated lymphoid cells. Most studies on NK cells in human neoplasia have dealt with reactivity against susceptible tissue culture lines, but freshly isolated human tumors are generally relatively resistant to these effector cells, particularly when autologous lymphoid cells are used. The resistance of fresh human neoplastic cells to NK activity has not been studied extensively and, together with the poor localization at the tumor site of NK effectors, it represents a major difficulty in envisaging a role for these cells in the control of established human neoplasia.