肿瘤血管生成抑制剂研究进展

肿瘤生长、侵袭、转移和复发是血管生成依赖性的,以肿瘤血管生成的各个环节为靶点,研制血管生成抑制剂,可有效地抑制肿瘤的转移和复发,成为肿瘤防治的新途径.本文就目前已进入临床试验的30多种血管生成抑制剂研究进展作一综述.     

肿瘤血管生成抑制剂研究进展

肿瘤生长、侵袭、转移和复发是血管生成依赖性的,以肿瘤血管生成的各个环节为靶点,研制血管生成抑制剂,可有效地抑制肿瘤的转移和复发,成为肿瘤防治的新途径。本文就目前已进入临床试验的30多种血管生成抑制剂研究进展作一综述。     

抗肿瘤血管生成,肿瘤免疫治疗与肿瘤微环境的研究进展

抗肿瘤血管生成已是临床上肿瘤治疗的常用方法.但是,在此治疗过程中,肿瘤也会逐渐对抗血管生成药物产生耐药,这可能与肿瘤微环境的改变有关.怎样进一步改善抗肿瘤血管生成治疗疗效是目前的热点问题.最近有研究认为将其与肿瘤免疫治疗相联合可能是一种相互增益的治疗策略.本文就抗肿瘤血管生成治疗及其耐药、肿瘤微环境与肿瘤免疫治疗的关系,抗肿瘤血管治疗联合肿瘤免疫治疗的最新进展,进行综述.以期为今后探索肿瘤治疗新靶点、寻找肿瘤治疗新模式提供思路及参考依据,从而最终造福于广大癌症患者.     

肿瘤血管生成与抗血管生成基因治疗

肿瘤血管生成是肿瘤生长浸润转移的关键步骤，其形成主要是促血管生成因子和抑制因子作用失衡的结果。以肿瘤血管生成为靶点的抗血管生成治疗作为肿瘤治疗新视野，已发展为重要的抗肿瘤策略。基因治疗则使抗血管生成治疗更具有靶向性，使这一治疗策略产生新的飞跃。本文就该领域研究情况作一综述。     

血管生成抑制因子的研究进展

血管生成与肿瘤的生长、侵袭和转移密切相关,目前,以抑制血管生成为靶点治疗肿瘤有望成为抗肿瘤新疗法之一。近年来,研究发现了多种内源性血管生成抑制因子,其中一些已进入了临床试验阶段。本文对内源性血管生成抑制因子的结构、功能、作用机制及其在肿瘤治疗中的应用进行综述。     

肿瘤血管生成拟态研究新进展

血管生成拟态是独立于血管生成的一种全新肿瘤血管模式。越来越多的研究发现血管生成拟态的形成机制和肿瘤细胞自身的可塑性及肿瘤干细胞关系密切,另外,肿瘤微环境如细胞外基质重塑、缺氧等在血管生成拟态形成过程中也有很重要的作用。近年来,血管生成拟态形成机制的相关研究已经取得了很大进展,为寻找抑制VM的关键作用靶点、筛选有效的治疗药物提供了新的思路和方向。本文就血管拟态的发现、形成机制及其在肿瘤治疗中的研究现状等方面做一综述。     

中介素与肿瘤

中介素可通过多种信号通路促进肿瘤血管生成,并受肿瘤细胞缺氧影响表达增加.近年来,国内外出现多项中介素与肿瘤发生、发展、侵袭之间相互关系及作用机制的研究,有望为肿瘤治疗提供新靶点.     

RhoC与肿瘤血管生成关系的研究进展

肿瘤血管生成是目前肿瘤治疗方面的研究热点。随着研究的不断深入,以RhoC为代表的Rho酶家族逐渐被发现与肿瘤血管生成存在密切关系。对RhoC与肿瘤血管生成关系进行研究,将有助于肿瘤血管生成新靶点的发现。     

肿瘤相关巨噬细胞对肿瘤新生血管生成的作用及其机制的研究进展

肿瘤相关巨噬细胞(TAM)在恶性肿瘤的发生、发展以及血管生成中发挥着重要作用.TAM被认为是肿瘤微环境(TME)的主要成分,具有促进肿瘤生长、侵袭、转移和肿瘤新生血管生成的作用.肿瘤基质中TAM的浸润水平、极化状态与患者预后密切相关,是肿瘤免疫治疗的潜在靶点.此外,肿瘤的生长依赖肿瘤新生血管生成,了解TAM在血管生成中...     

肿瘤血管异质性及其研究意义

肿瘤血管异质性是抗肿瘤血管生成研究的理论基础.肿瘤血管与正常血管相比,其表现形式、发生基础均存在显著差异.深入研究肿瘤血管异质性有助于发现新的分子诊断标记和治疗靶点.     

检测循环肿瘤细胞(CTC)在临床肿瘤诊断和治疗中的作用

有关循环肿瘤细胞的理论已有很长时间。肿瘤转移及复发的过程均是一个循环肿瘤细胞定植生长的级连放大的瀑布反应。目前肿瘤的发现和诊断仍高度依赖于影像学及肿瘤特异性血清标志物的方法,不能及时发现肿瘤的转移和复发。基于肿瘤细胞播散理论,检测循环肿瘤细胞可更早期有效发现肿瘤的早期转移和复发。本文对文献报道的检测循环肿瘤细胞在临床肿瘤诊断和治疗中的作用进行了总结,并与目前经典的标志物和影像学进行了比较。     

肿瘤相关物质联合检测试验对肿瘤的筛查及监控意义

目的　探讨肿瘤相关物质 (TumorSuppliedGroupofFactors ;TSGF)检测在肿瘤诊断及疗效观察中的意义。方法　用化学法测定163例恶性肿瘤患者 (A组 ) ,12 0例健康体检者 (B组 )及 2 2例良性肿瘤患者 (C组 )血清中的TSGF含量 ,并分析各观察组中TSGF的关系。结果　血清TSGF含量A组为 ( 67 4± 18 6)U/mL ;B组为 ( 5 1 7± 6 3 )U/mL ;C组为 ( 5 4 6± 7 5 )U/mL ,A组TSGF含量明显高于B组及C组 (P <0 0 1)。TSGF肿瘤诊断的总阳性率为 84 7% ,特异性为 96 3 % ;其中肺癌和大肠癌的阳性率分别为 90 7%、89 6% ;手术和化疗后随访的 2 3例大肠癌患者中 ,一年后有 1例TSGF持续阳性 ,后经确诊其为复发患者。结论　TSGF是一种广谱、灵敏 ,简便的肿瘤筛查指标 ,对肿瘤诊断、疗效评估、肿瘤复发判断等有重要的临床意义。     

MRI of pineal region tumors

The pineal region is a heterogeneous area that includes the pineal gland and several parapineal structures. Pineal region masses include germ cell tumors (GCTs), pineal parenchymal cell tumors, glioma, meningioma, metastases, and non-neoplastic masses such as pineal cysts, lipoma, epidermoid, vascular malformations. Although MRI has allowed an improvement in distinguishing true pineal masses from parapineal masses impinging into the region of the gland, it is still difficult to differentiate the pineal GCTs from pineal parenchymal tumors with only images, and the clinical informations such as age, sex, and the tumor markers are very important.     

溶瘤病毒抗神经胶质瘤治疗研究中的问题与对策

神经胶质瘤是人脑中最常见的原发性肿瘤，占中枢神经系统恶性肿瘤的81%，当前标准疗法仍是手术切除及术后放化疗。因神经胶质瘤具有高侵袭性、分子异质性、治疗后耐药肿瘤干细胞可再生，以及化疗药物难以通过血脑屏障（BBB）达到足够高的治疗浓度等特点，导致其预后非常差，患者中位存活期仅为15个月。近年来，新兴的溶瘤病毒免疫疗法治疗神经胶质瘤的研究备受关注并取得一定进展，但依然面临诸如BBB、免疫“冷”微环境、宿主抗病毒反应和肿瘤高度异质性等挑战。这些问题限制了溶瘤病毒疗法的深入发展及进一步应用，但也给基础与临床研究者带来新的研究机遇。因此，本文从穿越BBB、改善肿瘤微环境（TME）、调控溶瘤病毒介导的宿主免疫反应和适应肿瘤异质性等四个方面，阐述溶瘤病毒在抗神经胶质瘤治疗研究中的存在问题及对策。     

MicroRNAs在肿瘤相关成纤维细胞促进肿瘤发展进程中的作用

肿瘤相关成纤维细胞（CAFs）是肿瘤微环境（TME）中最主要的细胞组分之一,在肿瘤发生、进展中发挥重要作用。微小RNA（miRNAs）参与CAFs的转化与代谢重编程,并可调控CAFs 的干性及其介导的肿瘤细胞增殖、侵袭和化疗耐药等机制,在CAFs 的形成和CAFs 对肿瘤的促进作用中发挥重要功能;而CAFs 释放的miRNAs 可作为肿瘤的诊断、预后及用药选择的参考指标。因此探索miRNAs 在肿瘤细胞与CAFs 相互作用中的功能,揭示其作用机制,对于理解肿瘤的发生和发展具有重要意义;同时也可为新的肿瘤治疗策略提供研究方向。本文将对miRNAs在CAFs的形成及CAFs对肿瘤细胞调控中的作用加以介绍     

Peripheral primitive neuroectodermal tumor of the posterior mediastinum：A case report

Peripheral primitive neuroectodermal tumor （pPNET） is an extremely rare disease entity of malignant tumors belonging to the Ewing sarcoma family that usually occurs in children and adolescents. We describe a 41-year-old female who presented with right upper abdominal pain. Surgical resection and biopsy revealed small round-cell tumor. Combined with immunohistochemical analysis, pPNET was diagnosed. No evidence of recurrence was noted at 18 months postoperatively. Even thought pPNET is a highly malignant tumor, Wide tumor-free resection and multi-agent chemotherapy can also obtain good clinical outcomes.     

Outcome after surgical treatment of suspected gastrointestinal stromal tumors involving the duodenum: Is limited resection appropriate?

INTRODUCTION: Present surgical opinion is divided regarding the optimal method for the treatment of duodenal gastrointestinal stromal tumor (GIST) with some supporting the selective use of limited resection (LR) versus others who prefer pancreaticoduodenectomy (PD). METHODS: A retrospective review of 22 patients who underwent surgery for suspected GIST involving the duodenum. RESULTS: There were 15 GISTs, 1 leiomyosarcoma and 6 other non-GIST benign submucosal tumors. Seven patients underwent LR and seven underwent PD for GIST. The median follow-up was 42 (range, 2-174) months. Patients who underwent LR versus PD had similar mean disease-specific survival [144 (95% CI, 92-196) vs. 130 (95% CI, 82-127) months, P = 0.808] and recurrence rates (14% vs. 29%, P = 0.515). All recurrences occurred at distant sites. Comparison between LR versus PD demonstrated that LR was associated with a significantly shorter operation time [125 (range, 50-305) vs. 350 (range, 210-465) min., P = 0.001] but similar morbidity rate (23% vs. 43%, P = 0.357). Comparison between GIST and other benign tumors demonstrated that size was the only statistically significant distinguishing factor [8.5 (range, 2.5-18.0) vs. 2.5 (range, 1.5-8.0) cm, P = 0.014]. CONCLUSION: Benign non-GIST tumors may be distinguished from duodenal GIST as they are smaller in size. LR is a viable treatment option for suspected GIST involving the duodenum.     

已烯雌酚致新生鼠肺肿瘤模型的建立

Objective： To explore a economical and effective method for building lung tumor model induced by diethylstibestrol （DES）. Methods： The carcinogenic effect of neonatal mice treated by DES was studied. The newborn mice were divided into DES, Urethan （U） and U ＋ DES groups. U group was given in 500 mg/kg dose by ip at postnatal 14 day, DES group was administered by ip at the 1 d, 8 d, 15 d in the dose of 1/7, 2/7 and 4/7 LD50 of the day when they were injected respectively for DES （I）, DES （M）, DES （H） groups. Until 26 weeks, they were anatomized and checked the formation of tumors. The organ index, tumor incidence ratio and mean number of tumors were calculated. Results： Lung tumors were apparently induced in tested neonatal mice. The incidence of lung tumor of DES （L, M, H） groups were 16.7%, 22.4% and 43.1% respectively, the U ＋ DES （L, M, H） groups were 70.4%, 90.9% and 70.8% respectively, and the U group was 53.1%. The mean numbers of lung tumors of U ＋ DES （L, M） groups were higher than those of the DES （L, M） groups respectively （P 〈 0.05）. Conclusion： The higher ratio of lung tumor incidence had been induced by DES and U joined action to neonatal mice, which may be a useful and economical method to establish a lung tumor model induced by DES.     

IL-2及TNF的序贯应用对恶性肿瘤和宿主蛋白质代谢的影响

生物治疗被誉为肿瘤的第四种疗法,它已成为肿瘤研究的热点,并在肝癌临床中同样具有重要的战略地位。肝癌治疗的发展史中,曾使5年生存率有较大幅度提高的有50-60年代的大肝癌切除;70-80年代的小肝癌切除和目前的不能切除肝癌的缩小后切除。前两者是外科起主导作用的;后者则乃放、化疗、外科综合起作用,生物疗法亦参与起作用。预期在2000年前后,生物疗法将在肝癌治疗中着起举足轻重的作用。 1992年Gutterman将人癌的生物治疗分为4大类,即抗增殖的IFN-α、IFN-β、TGF-β……、免疫性的IL-2、IL-4、IFN-γ、INF、单抗……、造血生长因子CSF……及抗转移/抗血管生成TIMP1与2、胶原酶抑制剂……。而近年的迅速发展又极大地丰富了其内涵,诸如基因治疗、瘤苗、肿瘤多肽抗原、广义的抗体导向治疗等。     

Mechanisms of tumor escape from the immune system: adenosine-producing Treg, exosomes and tumor-associated TLRs

Human tumors utilize many different mechanisms of immunosuppression to prevent immune cells from exercising their antitumor activities. These mechanisms, which enable the tumor to escape from the host immune system and to progress, are being intensively investigated in hope of finding therapeutically safe and effective inhibitors able to counteract tumor-induced immunosuppression. Three of more recently discovered tumor-related suppression mechanisms, i.e. accumulations of adenosine-producing regulatory T-cells (Treg) in the tumor microenvironment, release by tumors of suppressive microvesicles (TMV) and expression of toll-like receptors (TLR) on the tumor cell surface, are described in this review. All contribute in a varying degree to creating a milieu favorable for the tumor and unfavorable for immune effector cells. Tumor escape has been a major problem in cancer immunotherapy and it has been held responsible for the failure of many immune interventions in cancer. For this reason, it is important to study and understand the various suppressive pathways human tumors utilize. Future antitumor immunotherapies are likely to include inhibitors of tumor-induced suppression with the goal of restoring antitumor immune responses in patients with cancer.