沙培林治疗36例恶性胸腔积液临床疗效观察

目的：观察沙培林治疗恶性胸腔积液的临床疗效。方法：经B超定位并行胸穿抽取胸腔积液，2周内隔日1次注入不同剂量的沙培林。结果：36例患者有效率91.7%，中位缓解期8.5个月。中位生存期11个月。主要毒副反应为不同程度发热。结论：沙培林能有效治疗恶性胸腔积液。     

顺铂联合沙培林治疗恶性胸腔积液临床观察

目的　探讨顺铂联合沙培林胸腔内局部应用治疗恶性胸腔积液的临床疗效。方法　 5 2例恶性肿瘤合并胸腔积液患者分为顺铂 沙培林组和顺铂组 ,采取胸腔内局部用药。结果　顺铂 沙培林组对恶性胸腔积液的有效率为 88 9% ,明显高于顺铂组有效率 (P <0 0 1)。结论　顺铂联合沙培林胸腔内部应用是治疗恶性胸腔积液的有效方法。     

沙培林治疗恶性胸腔积液的临床研究

观察沙培林治疗恶性胸腔积液的疗效及副作用。对 30例恶性胸腔积液患者应用沙培林腔内给药治疗 ,B超检查 ,观察效果。有效率达 66 7% ,不良反应主要是胸痛和发热。沙培林是治疗恶性胸腔积液的有效药物之一。     

顺铂联合沙培林治疗恶性胸腔积液临床观察

目的 探讨顺铂联合沙培林胸腔内局部应用治疗恶性胸腔积液的临床疗效。方法 52例恶性肿瘤合并胸腔积液患分为顺铂＋沙培林组和顺铂组，采取胸腔内局部用药。结果 顺铂＋沙培林组对恶性胸腔积液的有效率为88．9％，明显高于顺铂组有效率（P＜0．01）。结论 顺铂联合沙培林胸腔内部应用是治疗恶性胸腔积液的有效方法。     

沙培林治疗恶性胸腔积液的临床研究

观察沙培林治疗恶性胸腔积液的疗效及副作用。对30例恶性胸腔积液患者应用沙培林腔内给药治疗，B超检查，观察效果。有效率达66．7％，不良反应主要是胸痛和发热。沙培林是治疗恶性胸腔积液的有效药物之一。     

康莱特联合沙培林治疗老年恶性胸腔积液的临床观察

目的 观察康莱特联合沙培林治疗老年恶性胸腔积液的近期疗效、生活质量提高情况.方法 56例诊断为肺癌恶性胸腔积液的老年患者随机分组,治疗组28例应用康莱特的同时给予沙培林胸腔灌注治疗,对照组28例仅用沙培林胸腔灌注治疗,4周后观察疗效.结果 有效率(CR PR)治疗组为89.3%,对照组为85.7%,治疗组疾病控制率高于对照组,但差异无统计学意义,而治疗组较对照组的生活质量明显提高,差异有统计学意义(P相似文献   

沙培林治疗恶性胸腔积液疗效观察

恶性胸腔积液是晚期恶性肿瘤常见的并发症之一 ,化疗药物是治疗恶性胸腔积液的主要方法 ,但有些患者因体质虚弱、肝肾功能异常不能接受胸腔灌注化疗药物 ,我们采用沙培林治疗恶性胸腔积液取得较好的疗效 ,总结报告如下。1　临床资料1.1　一般资料共 30例 ,其中男 2 6例 ,女 4例 ;年龄 35～ 6 8岁 ,均有病理学及细胞学诊断 ,原发性肺癌 2 3例 ,乳腺癌 4例 ,食管癌 4例 ,随机分为沙培林组 2 0例 ,化疗组 10例。1.2　治疗方法沙培林组 :先行青霉素皮试 ,阴性者方可使用。尽量抽尽胸腔积液后 ,每周注入沙培林 1次 ,治疗 2～ 3次 ,剂量为 2ＫＥ、…     

局部灌注沙培林和羟基喜树碱治疗恶性胸腔积液

[目的]观察沙培林(0K-432)和羟基喜树碱(HCPT)治疗恶性胸腔积液的近期临床疗效。[方法]对62例恶性胸腔积液患者采用胸腔置入贝朗可分裂中心静脉管持续引流，胸腔积液排放完后，给予沙培林5KE胸腔内注入，dl，HCPT30mg胸腔内注入，d2，每周2次，观察临床疗效与不良反应。[结果]沙培林与HCPT联合治疗恶性胸腔积液总有效率为88．7％，主要不良反应为发热和骨髓抑制。[结论]胸穿置管引流局部灌注沙培林和羟基喜树碱治疗恶性胸积液有较好的近期临床疗效，毒副反应可以耐受。     

电视胸腔镜胸膜固定术治疗恶性胸腔积液的临床疗效及影响因素

目的:探讨电视胸腔镜胸膜固定术治疗恶性胸腔积液的临床效果,总结影响恶性胸腔积液的相关因素。方法:回顾性分析2011年1月至2013年1月87例恶性胸腔积液患者的临床资料。全部采用电视胸腔镜胸膜固定术治疗,观察其术后的临床效果,并分析影响中位生存时间的因素。结果:电视胸腔镜胸膜固定术治疗恶性胸腔积液的总有效率为63.2%。不良反应总发生率为9.1%。Karnfsky生活质量稳定以上的占97.7%。胸膜肥厚和包裹积液的总发生率为19.5%。肿瘤类型、CEA、LDH、蛋白质含量、沙培林灌注、胸水Glu水平均是电视胸腔镜胸膜固定术治疗恶性胸腔积液的主要影响因素（P<0.05）。结论:电视胸腔镜胸膜固定术治疗恶性胸腔积液临床效果确切,而肿瘤类型、CEA、LDH、蛋白质含量、沙培林灌注、胸水Glu水平是影响预后的相关因素。     

中心静脉导管留置引流并胸腔内注药治疗恶性胸腔积液42例临床观察

目的探讨用中心静脉导管行胸腔置管引流加药物灌注治疗恶性胸腔积液的临床疗效。方法对我院住院确诊的42例恶性胸腔积液患者,用中心静脉导管行胸腔置管引流干净后给予胸膜腔内不同药物灌注治疗,于注药前及注药后4周观察患者症状、毒副反应并判断疗效。结果 42例恶性胸腔积液患者中治疗后获CR18例,PR17例,NR7例,总有效率为83.3%,均无严重毒副反应发生。结论中心静脉导管行胸腔置管引流后灌注丝裂霉素＋沙培林或顺铂＋沙培林治疗恶性胸腔积液有一定疗效且毒副反应少,是一种较好的治疗选择。     

Farnesyltransferase inhibitors: antineoplastic properties, mechanisms of action, and clinical prospects

Farnesyltransferase (FTase) inhibitors are among the current wave of molecularly targeted anti-cancer agents being used to attack malignancy in a rational manner. A large body of preclinical data indicates that FTase inhibitors block cancer cell proliferation through both cytostatic and cytotoxic effects. Interestingly, FTase inhibitors have rather limited effects on normal cell function, suggesting that they may target unique aspects of cancer cell pathophysiology. The development of FTase inhibitors was predicated on the discovery that the Ras oncoproteins must be post-translationally modified to transform cells. However, recent work indicates that the anti-neoplastic effects of FTase inhibitors depend on altering the post-translational modifications of non-Ras proteins as well. In particular, a critical target protein that responds to FTase inhibition by blocking tumor cell growth is RhoB, an endosomal Rho protein that functions in receptor trafficking. In this review, we survey the biological foundations for the clinical development of FTase inhibitors, and consider some of the latest mechanistic studies that reveal how these agents affect cellular physiology.     

Targeting tumor vasculature with homing peptides from phage display

Tumor vasculature expresses a number of molecular markers at much lower levels than those seen in the blood vessels of normal tissues, and in some cases, such markers are undetectable. The presence of these markers relates to angiogenesis; the same markers are shared by all blood vessels undergoing angiogenesis. The endothelial cells, pericytes and smooth muscle cells, and the vascular extracellular matrix in angiogenic vessels can each express such markers. Molecularly, they represent vascular growth factor receptors, cell adhesion proteins and their receptors. Screening of phage display libraries for peptides that home to tumor vasculature when injected into mice has recently provided a new tool for analyzing the distinguishing features of tumor vasculature. Tumor-homing peptides isolated in this manner, as well as an antibody against a form of fibronectin expressed in tumor blood vessels, have been found to serve as targeting devices to concentrate drugs and other therapeutic materials to tumors in in vivo models. Such a targeting strategy can therefore potentially improve the efficacy of drugs and reduce their side effects.     

Identification of EBV transforming genes by recombinant EBV technology

Epstein-Barr virus (EBV) is able to infect primary B-lymphocytes but usually does not proceed to replicate more virions. Instead, EBV persists as an incomplete virus and expresses 12 gene products that transform the growth of these cells into continuously proliferating lymphoblastoid cell lines. Because EBV is associated with several human malignancies, there is intense interest in delineating the molecular functions of these EBV gene products in transformation. This review focuses on the recombinant EBV technologies that have been developed to introduce specific mutations into EBV and test the functions of these EBV genes in primary B-lymphocyte growth transformation.     

Matrix metalloproteinases in tumor invasion and metastasis

Extensive work on the mechanisms of tumor invasion and metastasis has identified matrix metalloproteinases (MMPs) as key players in the events that underlie tumor dissemination. Studies using natural and synthetic MMP inhibitors, as well as tumor cells transfected with cDNAs encoding the MMPs characterized thus far have provided compelling evidence that MMP activity can induce or enhance tumor survival, invasion and metastasis. Because of the ability of MMPs to degrade extracellular matrix (ECM) proteins, the principal mechanism whereby MMPs promote tumor development has been thought to be the proteolytic breakdown of tissue barriers to invasion and the associated facilitation of circulating tumor cell extravasation. However, recent evidence stemming from the use of novel experimental approaches indicates that MMPs do not play a major role in the process of extravasation itself. Rather, they appear to promote intravasation (the process of penetrating the circulation following invasion of blood vessels) and regulate the relationship between tumor cells and host tissue stroma subsequent to extravasation. In addition, the discoveries that a growing number of proteolytically active MMPs may localize to the cell surface in association with adhesion receptors, and that MMP substrates include latent cytokines and growth factors, provide a new conceptual framework for the mechanisms whereby MMPs influence tumor behavior.     

New aspects of integrin signaling in cancer

Members of the integrin family of cell adhesion receptors influence several important aspects of cancer cell behavior, including motility and invasiveness, cell growth, and cell survival. Engagement of integrins with extracellular matrix (ECM) proteins can activate members of the Rho-family of small GTPases; conversely, Rho- and Ras-family proteins can influence the ability of integrins to bind their ligands. These events impinge on the control of cell motility, and ultimately on invasive and metastatic behavior. Integrin engagement with ECM also has important effects on cell survival, particularly for cells of epithelial origin. In some cases, specific integrins have selective effects on the efficiency of signal transduction in cell survival pathways.     

Role of LMP1 in immune control of EBV infection

The Epstein-Barr virus (EBV) encoded latent membrane protein (LMP1) plays a crucial role in the long-term persistence of this virus within the cells of the immune system. Not only is this protein critical for the transformation of resting B cells by EBV, it also displays pleiotropic effects on various cellular proteins expressed in the host cell. These include up-regulation of expression of B cell activation antigens, adhesion molecules and various components of the antigen processing pathway. Here we discuss how LMP1 acts like an expression 'switch' which, depending on the stage of EBV infection, manoeuvres various pathways that either modulate the immune system towards or against its survival.     

腹部压块对膈肌运动影响的研究

目的 :研究腹部压块对膈肌运动的影响。方法 :选择拟行立体适形放疗患有肺癌或肝脏肿瘤的患者 2 0例。按治疗体位仰卧于体部立体放疗定位负压袋内 ,待患者呼吸平稳后 ,将灯光野的中心点置于膈顶运动的最低点 ,在膈肌运动至最高位时拍摄照片 ,测量膈肌运动的最大幅度 ;然后 ,将心形腹部压块放置于患者剑突下 ,并用定位框架的腹带交叉固定 ,按压程度以不引起患者呼吸困难或其他不适为标准 ,5min后按上述方法再次测量膈肌运动的最大幅度。结果 :2 0例患者未加腹部压块的运动幅度为0 6 2～ 2 6 7cm ,平均 (1 4± 0 6 4)cm ,加腹部压块后的膈肌运动幅度为 0 2 8～ 2 0 8cm ,平均 (1 0±0 5 5 )cm ,加腹部压块后膈肌运动幅度平均减小 (0 4± 0 34)cm ,P =0 0 0 0。加腹部压块后 90 % (18/2 0 )的患者膈肌运动幅度受到不同程度的限制 ,但有 10 % (2 /2 0 )的患者膈肌运动幅度增加。结论 :腹部压块可使大部分患者膈肌运动的幅度减小 ,但少部分患者例外 ,即腹部压块并不能使所有膈肌周围肿瘤的照射容积减少。建议在制定放射治疗计划前应预先进行测量和评价     

ABCG2在肺癌中表达的定量研究

目的 观察ABCG2在肺癌和癌周肺组织的表达,从量化角度阐明其在肺癌组织中表达的病理学意义.方法 常规石蜡包埋、HE切片确诊,用免疫组化SP法检测ABCG2在肺癌和癌周肺组织的定位和表达,用LeicaQ500MC图像分析系统对其表达强度进行定量分析,并用表达的阳性单位(positive unit PU)反映其表达强度.结果 ABCG2蛋白在肺癌和癌周正常肺组织中的表达主要定位在细胞质和细胞膜.在癌周正常肺组织的支气管和细支气管上皮呈弥漫表达,腺上皮呈灶性表达;肺鳞癌和肺腺癌弥漫或大片表达,肺鳞癌表达的PU值高于肺腺癌(P＜0.001),肺大细胞癌和肺小细胞癌不表达,PU值接近于零.癌周肺组织表达的PU值高于各型肺癌(P＜0.05).ABCG2蛋白表达的PU值在肺癌原发灶和转移灶之间无差别(P＞0.05),且与肺癌患者的性别、年龄、转移和TNM分期未见明显相关性(P＞0.05),与肺癌分化程度有关(P＜0.001).分化程度越高,PU值越高,但高分化肺癌和癌周肺组织的表达PU值差异无显著性(P＞0.05).结论 ABCG2蛋白表达程度与肺癌类型及分化程度具有相关性,可能成为判断其指标之一.     

Telomerase and human tumorigenesis

Human cancer cells, unlike their normal counterparts, have shed the molecular restraints to limited cell growth and are immortal. Exactly how cancer cells manage this at the molecular level is beginning to be understood. Human cells must overcome two barriers to cellular proliferation. The first barrier, referred to as senescence, minimally involves the p53 and Rb tumor-suppressor pathways. Inactivation of these pathways results in some extension of lifespan. However, inactivation of these pathways is insufficient for immortalization. As normal cells undergo repeated rounds of DNA replication, their telomeres shorten due to the inability of traditional DNA polymerases to completely replicate the end of the chromosomal DNA. This shortening continues until the cells reach a second proliferative block referred to as crisis, which is characterized by chromosomal instability, end-to-end fusions, and cell death. Stabilization of the telomeric DNA through either telomerase activation or the activation of the alternative mechanism of telomere maintenance (ALT) is essential if the cells are to survive and proliferate indefinitely. Conversely, loss of telomere stabilization by an already-immortalized cell results in loss of immortality and cell death. Together this indicates that telomere maintenance is a critical component of immortality. In this review we attempt to describe our current understanding of the role of telomere maintenance in senescence, crisis, and tumorigenesis.     

Post-translational regulation of COX2 activity by FYN in prostate cancer cells

While increased COX2 expression and prostaglandin levels are elevated in human cancers, the mechanisms of COX2 regulation at the post-translational level are unknown. Initial observation that COX2 forms adduct with non-receptor tyrosine kinase FYN, prompted us to study FYN-mediated post-translational regulation of COX2. We found that FYN increased COX2 activity in prostate cancer cells DU145, independent of changes in COX2 or COX1 protein expression levels. We report that FYN phosphorylates human COX2 on Tyr 446, and while corresponding phospho-mimetic COX2 mutation promotes COX2 activity, the phosphorylation blocking mutation prevents FYN-mediated increase in COX2 activity.