鼻咽癌放疗后放射性脑干损伤的MRI表现

目的分析鼻咽癌患者放疗后发生放射性脑干损伤的MRI表现特征。方法对37例鼻咽癌放疗后发生放射性脑干损伤患者的MRI资料进行复阅,对MRI检查序列包括T1WI、T2WI、FLAIR以及增强扫描序列进行分析,明确放射性脑干损伤的病变部位、范围、信号强度和增强后病灶强化等的形态。结果37例放射性脑干损伤患者,病变位于脑桥19例,中脑1例,延髓3例,脑桥＋中脑6例,脑桥＋延髓5例,中脑＋脑桥＋延髓3例。病灶在MRI上TIWI表现为等信号或低信号,TaWI表现为高信号,FLAIR表现为低、高混杂信号,增强后无明显强化者9例,强化者28例。强化方式：均匀斑片状强化者12例、不均匀环形强化者16例。结论MRI可以清晰地显示放射性脑干损伤的病灶,MRI对于诊断放射性脑干损伤有着重要价值,为临床治疗提供参考。     

鼻咽癌放疗后放射性脑干损伤的MRI表现

目的分析鼻咽癌患者放疗后发生放射性脑干损伤的MRI表现特征。方法对37例鼻咽癌放疗后发生放射性脑干损伤患者的MRI资料进行复阅,对MRI检查序列包括T1WI、T2WI、FLAIR以及增强扫描序列进行分析,明确放射性脑干损伤的病变部位、范围、信号强度和增强后病灶强化等的形态。结果 37例放射性脑干损伤患者,病变位于脑桥19例,中脑1例,延髓3例,脑桥+中脑6例,脑桥+延髓5例,中脑+脑桥+延髓3例。病灶在MRI上T1WI表现为等信号或低信号,T2WI表现为高信号,FLAIR表现为低、高混杂信号,增强后无明显强化者9例,强化者28例。强化方式:均匀斑片状强化者12例、不均匀环形强化者16例。结论 MRI可以清晰地显示放射性脑干损伤的病灶,MRI对于诊断放射性脑干损伤有着重要价值,为临床治疗提供参考。     

鼻咽癌放疗后放射性脑干和脊髓损伤的磁共振表现

背景与目的:鼻咽癌(nasopharyngealcarcinoma,NPC)放射治疗后脑干和颈髓放射性损伤的诊断相当重要。磁共振(magneticresonanceimaging,MRI)用于诊断鼻咽癌放疗后放射性脑损伤已有较多报道,但脑干和颈髓放射性损伤的MRI表现文献报道较少。本研究旨在分析鼻咽癌放疗后脑干和颈髓放射性损伤的MRI特征。方法:对60例鼻咽癌患者在放射治疗后6个月至5年内进行了MRI检查,MRI检查序列包括T1-weightedimage(T1WI)、T2-weightedimage(T2WI)、fluidattenuatedinversionrecovery(FLAIR);所有患者均做了MRI增强扫描。结果:6例为颈髓放射性损伤;54例为脑干放射性损伤,其中脑桥20例,桥脑基底部与延髓上段26例,中脑受累3例,延髓5例。病灶在MRI上T1WI表现为等信号和低信号,T2WI上为高信号,增强后病灶无强化者11例(18.3%),强化者49例(81.7%)。强化者有2种强化形式:均匀斑片状强化(21例,42.9%)和不均匀的既有环形又有斑片状的强化(28例,57.1%)。结论:MRI可以清晰地显示脑干和脊髓放射性损伤的病灶,结合病史可以确诊。     

鼻咽癌放射治疗后脑损伤的临床研究

目的探讨鼻咽癌放射治疗后脑损伤的临床特点、CT及MRI表现、诊断、治疗及预后因素。方法回顾性分析1991年1月至2004年4月收治的51例鼻咽癌放射治疗后脑损伤患者的临床病例资料。结果男性患者36例,女性15例,颞叶损伤的中位潜伏期为3年,脑干损伤为1年8个月。本组颞叶型18例(35.3%),脑干型19例(37.3%),小脑型2例(3.9%),混合型12例(23.5%)。MRI主要表现为信号异常,T1WI以低信号为主,T2WI为高信号。35例早期用激素、大量维生素等药物治疗者,对颞叶损伤的有效率75.0%,脑干损伤为59.1%。44例随访3个月～10年,20例在出现神经症状7个月～6年内死亡,其中死于脑损伤10例,肿瘤转移5例,自杀2例,鼻咽部大出血1例,死因不明2例。现生存25例,出现神经症状后生存3个月～10年,13例能生活自理,12例需人照顾。结论放射性脑损伤首选MRI检查;以颞叶损伤相比,脑干损伤潜伏期短,症状较重,治疗效果较差。放射性脑损伤缺乏特异性的治疗手段,它的发生与照射剂量、照射体积及分次剂量有关。     

鼻咽癌放疗后脑干放射性脑病的诊断

 目的 探讨鼻咽癌放射治疗后脑干放射性脑病（REP）的临床诊断和磁共振（MRI）表现。方法 回顾性分析12例鼻咽癌放射治疗后REP患者的临床资料和MRI资料。结果　脑干REP主要累及脑桥。T1WI为低信号或等信号，T2WI为高信号，T1WI+ GdDTPA增强扫描可见点状或不规则环状强化，病灶均小于2 cm，周围水肿轻，无占位效应。结论　鼻咽癌放射治疗后脑干REP的MRI表现有一定的特征性，可作为REP诊断的主要方法。     

鼻咽癌放射治疗后脑脊髓损伤的临床和影像学诊断

目的　探讨鼻咽癌患者放射治疗后脑脊髓放射性损伤的临床和影像学诊断。方法　对 32例鼻咽癌放射治疗脑脊髓放射性损伤患者的临床表现、CT及MRI表现进行回顾性分析。结果　 32例中共发现 4 5个损伤病灶 ,颞叶 30个 (占脑损伤病灶的 70 % ) ,脑干 13个 ,颈段脊髓 2个。其中 6例放射性颞叶损伤无临床症状。CT对颞叶放射性损伤的检出率为 87% ,对脑干损伤的检出率仅 2 9%。放射性颞叶损伤在CT图象上主要表现为指状低密度。MRI检查T1WI图象上放射性脑脊髓损伤均表现为低或等信号 ,T2 WI图象上为高信号或混合信号 ,颞叶损伤可伴有周围指状分布水肿信号 ,86 %病灶有增强效应 ,中间有不增强区。结论　放射性脑脊髓损伤的临床表现无特征性 ,亦可无症状 ,CT及MRI表现具有一定的特征性 ,结合病史可做出诊断。MRI在诊断脑干、脊膜损伤上优于CT。     

鼻咽癌海绵窦侵犯调强放疗后放射性颞叶损伤的临床分析

目的 探讨海绵窦受侵的局部晚期鼻咽癌行调强放疗后发生放射性颞叶损伤的临床特征、MRI表现、放疗剂量和预后。方法 回顾性分析2006年8月至2011年9月收治的10例行根治性调强放疗的海绵窦受侵局部晚期鼻咽癌患者,统计放疗计划中患侧颞叶受照射的总体积和剂量体积D1 ml、Dmax、Dmean,并随访所有患者治疗后的情况,分析发生放射性颞叶损伤后的临床特征、MRI表现及预后。结果 10例患者均行根治性调强放疗,患侧颞叶受照射的总体积为（104.31±13.091） ml,D1 ml为（78.657±2.918）Gy,Dmax为（78.298±3.498）Gy,Dmean为（29.488±8.891）Gy。全组患者于治疗后2～4年出现放射性颞叶损伤,其MRI表现均为T1WI高信号强化结节或片状强化灶,T2WI伴有不同程度的水肿带。随访至2016年8月,2例患者死亡;2例临床症状较重,迁延时间长,治疗后症状改善不明显,且MRI仍可见强化灶和水肿带;2例患者经对症处理后临床症状及MRI检查均明显好转;4例患者病情趋于稳定,其中2例患者的恢复期MRI提示小囊性灶形成。结论 海绵窦受侵的局部晚期鼻咽癌患者行调强放疗后发生放射性颞叶损伤与肿瘤侵犯范围、靶区勾画范围、颞叶受照射的体积及剂量有关。     

鼻咽癌放射治疗后放射性脑病的临床分析

目的 :探讨鼻咽癌放射治疗后放射性脑病的临床特点、治疗及预后。方法 :对我院收治的 4 6 9例鼻咽癌患者中 ,采用面颈联合野 36～ 4 0Gy后缩野改耳前野加鼻前野或耳后野 ,常规放疗 4 0 6例 ,中位剂量 70 (6 6～ 74 )Gy ,后程加速超分割 32例 ,中位剂量 76 (70～ 80 )Gy ,超分割 31例 ,剂量 76 8Gy。 结果 :18例发生放射性脑病病变部位 :颞叶 15例 ,双侧 4例 ,单侧 11例 ,脑桥 3例。潜伏期 :单程放射治疗中位潜伏期 33(2 2～ 77)个月 ;再程放射治疗中位潜伏期 8 5 (6～ 2 8)个月。全组随访率 10 0 % ,16例仍存活 ,2例死于放射性脑病。结论 :鼻咽癌放射性脑病与剂量及照射野设计有关。MRI为其重要的诊断方法 ,PET可作为鉴别诊断的方法之一。尽早进行激素、脱水、扩血管和脑细胞营养药等治疗可有一定效果 ,但对病情反复 ,且有手术指征的患者尽早切除病灶可获良效     

鼻咽癌放疗后放射性脑病的MRI表现

目的:探讨鼻咽癌放射治疗后放射性脑病的MRI表现.方法:分析31例经病理证实鼻咽癌放射治疗后,放射性脑病MRI的T1WI及T2WI和增强表现及临床表现.结果:放射性脑病的临床表现为头痛、头晕、视力障碍、肢体麻木、无力或瘫痪及颅神经损伤症状.MRI显示大脑及脑干内斑片状改变,自旋回波T1WI病灶呈低或等信号,自旋回波T1WI呈等高混杂信号.增强扫描病灶区无强化者5例,斑点状强化者2例,不规则花环状强化者24例.占位效应与病灶大小不相称.12例复查,2例病灶消失,8例病灶形态及位置无变化.2例病灶增大.结论:MRI可显示放射性脑病的特征,是一种有效的检查方法.     

鼻咽癌放疗后放射性脑病的临床观察

目的：分析鼻咽癌放疗后放射性脑病发生的相关因素及其诊断、治疗和预后，并探索防治措施。方法：回顾性分析鼻咽癌放疗后放射性脑病23例临床病理资料，大部分采用CT和／或MRI诊断，1例据病理诊断。结果：本组脑耐受量为1116～1348btu，颞叶型潜伏期为20个月～9年，脑干型为11个月～4年半。死亡6例，其中急性者2例，延迟性者4例(脑干型3例，颞叶型1例)。结论：1)受照射脑体积、总剂量、分次剂量、脑组织敏感性是放射性脑病发生相关因素；2)CT和MRI是诊断放射性脑病的主要方法；3)急性者预后差；脑干型潜伏期短，预后较颞叶型差，潜伏期越长预后越好。     

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.