常规分割三维适形放疗对不可切除的原发性肝细胞癌的疗效分析

目的 探讨常规分割三维适形放疗对不可切除的原发性肝细胞癌的疗效.方法 用8MVX射线对52例不可切除的原发性肝细胞癌患者进行三维适形放疗,单次剂量2 Gy,每周5次,3.6～5.6周,总剂量36 ～ 66 Gy.CT扫描肿瘤最大直径、评价疗效、记录生存期及评估不良反应.结果 52例不可切除的原发性肝细胞癌患者中,完全缓解2例,部分缓解34例,总有效率为69.2％;放射性肝病发生率为1.92％.50 Gy以上和50 Gy以下剂量组缓解率分别为76.9％与46.2％(x2=10.72,P＜0.05).中位生存时间为10.5个月,1、2、3和4年生存率为57.7％、34.6％、23.1％和9.61％;未出现3或4级急性放射性损伤.结论 常规分割三维适形放疗治疗不可切除的肝细胞癌有效率高,不良反应轻.     

透明细胞型原发性肝细胞癌CT表现

透明细胞型原发性肝细胞癌是肝细胞癌的一种少见类型,其病理特征与普通肝细胞癌明显不同,细胞内含大量中性糖原或脂肪,相关其影像诊断研究的报道较少[1].笔者回顾性分析经病理证实的透明细胞型原发性肝细胞癌8例,以提高对本病的认识和影像诊断水平.     

索拉非尼治疗晚期肝细胞癌16例

原发性肝细胞癌是常见的恶性肿瘤之一,在全球占恶性肿瘤发病率第6位,占死因第3位。肝细胞癌患者大多有肝硬化基础疾病,肝功能较差,化疗和放疗使患者受益很少。索拉非尼（商品名“多吉美”,德国拜耳公司产品）,是一种小分子多靶点药物,近几年已广泛应用于临床。我科2008—12至2011—05有16例晚期肝细胞癌通过索拉非尼治疗取得了一定疗效,改善了患者生活质量,不良反应较轻,患者耐受性较好。     

TAE治疗原发肝细胞癌（对不同组织胞学类型疗效的初步研究）

目的：通过对一组１５７例经组织细胞学检查证实的原发性肝细胞癌患者生存资料及影像学资料的分析，初步研究经导管动脉栓塞（ＴＡＥ）对不同组织细胞学类型肝细胞癌的治疗效果，材料与方法：８种不同组织细胞学类型的资料较完整的原发性肝细胞癌患者，共计１５７例，分别接受单纯ＴＡＥ，单纯手术或ＴＡＥ＋手术切除治疗，对上述病分别按照不同组织细胞学类型及不同治疗方法进行生存资料和影像学资料分析，结果：本组原发性肝细胞癌     

双期动态增强螺旋CT评价原发性肝细胞癌边缘血供情况

目的:应用螺旋CT双期扫描研究原发性肝细胞癌(primary hepatocellular carcinoma,PHCC)边缘的血供情况.方法:对52例经活检、手术及血管造影诊断的原发性肝细胞癌经螺旋CT全肝平扫及动脉期、门脉期双期增强扫描的分析.动脉期的延迟时间为18～20s,门脉期为50～60s.结果:①原发性肝细胞癌4种肿瘤边缘CT征象分型通过双期动态增强螺旋CT很好显示;②CT平扫显示边缘模糊的病灶,在门脉期大部分范围减小,而在动脉期范围不变.动脉期能很好的反映肿瘤的大小和形状;③原发性肝细胞癌在双期边缘的强化特点可以反映其病理组织学的特点.结论:螺旋CT双期动态扫描能够很好的展示原发性肝细胞癌的CT特点及其血供情况.     

肝细胞癌合并门静脉癌栓的联合放疗的综合治疗进展

肝细胞癌发生及发展过程中易侵犯门静脉形成门静脉癌栓,由于预后极差且缺乏有效的治疗手段,是影响肝癌整体疗效提高的瓶颈。肝癌合并门静脉癌栓的最佳治疗方法仍存在争议。随着技术的发展,放疗对于门静脉癌栓治疗的安全性和有效性已得到广泛证实。个体化及综合治疗的进一步优化是未来的研究方向。本文探讨肝细胞癌合并门静脉癌栓放疗及综合治疗...     

肝癌的介入诊疗(一)

正肝癌分原发性肝癌(包括肝细胞癌、胆管细胞癌、混合型肝癌)和转移性肝癌,成人原发性肝癌的最常见类型是肝细胞癌。在全球范围内,肝细胞癌在癌症相关死亡的常见原因中居第3位,且发病率持续上升[1]。"肝癌"常被用来指代"肝细胞癌",而原发     

肝癌CT表现的分子生物学基础

肝细胞癌的生物学行为，可通过CT来反映，从而作出较明确的判定。随着现代分子生物学技术的发展，对肝细胞癌的认识已深入到基因水平，这有助于解释肝细胞癌影像学表现的多样性和复杂性。目前，影像学（大体形态学）和相关肿瘤基因（微观）的系统研究已成为影像学研究的热点。本对肝细胞癌相关基因和抑癌基因的研究进行了回顾与综述，以期进一步认识肝细胞癌的分子生物学基础。     

直肠癌术前放疗对癌巢内浸润T淋巴细胞亚群的影响

 目的 观察直肠癌术前放疗对癌巢内浸润T淋巴细胞亚群的影响.方法 选择1999年1月～2007年8月我院直肠癌单纯术前放疗患者1 07例入组研究,术前放疗30 Gy/10 f/12 d,2周后手术.回顾分析术前放疗对癌巢内T淋巴细胞亚群CD3、CD4、CD8数量的影响,并进行放疗前后自身对照分析.结果 放疗后CD3比放疗前显著增多(P<0.01),放疗后CD8数量显著下降(P<0.05), 放疗后CD4/CD8比放疗前升高(P<0.01).放疗后CD3数量级别与直肠癌术前放疗近期局部疗效关系密切(P<0.01).结论 直肠癌术前放疗后的癌巢组织中CD3 浸润数目增多,CD4/CD8比值升高,放疗后CD3数量与近期局部疗效相关.     

载药微球经导管肝动脉化疗栓塞治疗肝脏恶性肿瘤研究进展

肝癌是目前临床上常见的消化系统恶性肿瘤,包括原发性肝癌与继发性肝癌,原发性肝癌主要分为肝细胞癌与胆管细胞癌,继发性肝癌则多源于结直肠癌的肝转移。肝癌的治疗手段包括手术切除、肝移植、消融治疗、经导管肝动脉化疗栓塞(TACE)、经肝动脉化疗灌注、靶向治疗及免疫治疗等。根据巴塞罗那分期(BCLC)及中国《原发性肝癌诊疗规范(2019年版)》,TACE可作为无法手术切除的中期肝细胞癌患者的首选治疗方案。随着载药微球的兴起与发展,载药微球-TACE(D-TACE)开始在各个分期的肝癌治疗中崭露头角。本文就TACE尤其是D-TACE在肝细胞癌、胆管细胞癌及肝转移瘤中的应用,TACE与其他治疗方式的临床获益及不良反应,以及TACE治疗后的肿瘤复发和影响预后的分子机制进行综述。     

食管癌放射抗拒关键基因及通路的生物信息学分析

目的 寻找食管癌放射抗拒关键分子及通路,从分子水平揭示食管癌放射抗拒发生机制。方法 从基因芯片公共数据库GEO中下载食管癌放射抗拒相关芯片数据（GSE61772,GSE61620）;进一步运用GEO2R进行差异基因分析,利用DAVID、String等分析软件对差异基因进行生物信息学分析。RT-PCR技术检测差异基因在不同放射敏感性细胞中表达差异。结果 两组芯片数据中共筛选出49个差异基因,这些基因参与生物学过程主要集中在调节多细胞生物合成、离子转运、DNA合成、代谢、调节细胞增殖等。差异基因涉及的主要生物学通路是Wnt信号通路。12个差异基因间存在相互作用关系,关键节点为CHN2。CHN2基因在不同放射敏感性食管癌细胞中表达未见明显差异。结论 包括CHN2在内的49个差异基因可能与食管癌放射抗拒发生相关, Wnt信号通路在其中具有重要作用。     

Dexamethasone-induced radioresistance occurring independent of human papilloma virus gene expression in cervical carcinoma cells

Background

Inactivation of p53 by binding to simian virus 40-T antigen (SV40-T) and human papilloma virus type 16 protein E6 (HPV 16 E6) in transfected human diploid fibroblasts causes enhanced radioresistance. The aim of this study was to investigate the role of HPV 18 E6 and E7 gene products with respect to radiosensitivity of two cervical carcinoma cell lines.

Materials and Methods

The two cervical carcinoma lines C4-1 and SW 756 were used in which treatment with dexamethasone allows to modulate expression levels of HPV 18 E6 and E7 genes: upregulation in C4-1, downregulation in SW 756. Effects of treatment with dexamethasone on plating efficiency and radiosensitivity were assessed using a clonogenic assay.

Results

Treatment with dexamethasone increased plating efficiency of the C4-1 cells, but did not affect plating efficiency of SW 756 cells. Treatment with dexamethasone induced enhanced radioresistance in both cell lines. Thus, in C4-1 cells the observed changes in radioresistance correlate to the enhancement in expression of HPV 18 genes E6/E7, whereas in SW 756, a reduced expression correlates negatively with the enhanced radioresistance.

Conclusions

In C4-1 and SW 756 cells, treatment with dexamethasone induces radioresistance, and changes in expression levels of HPV 18 genes E6 and E7 do not correlate with the changes in radiosensitivity. Dexamethasone-induced radioresistance has previously been observed in HeLa cells, another human cervical carcinoma cell line. This leads us to speculate that dexamethasone-induced radioresistance may be important in certain clinical situations, and that therefore, the phenomenon deserves further study.     

Dexamethasone-Induced Enhancement of Resistance to Ionizing Radiation and Chemotherapeutic Agents in Human Tumor Cells

BACKGROUND: Dexamethasone-induced changes in radioresistance have previously been observed by several authors. Here, we examined effects of dexamethasone on resistance to ionizing radiation in 10 additional human cell lines and strains, and on resistance to carboplatin and paclitaxel in 13 fresh tumor samples. MATERIAL AND METHODS: Eight human carcinoma cell lines, a glioblastoma cell line and a strain of normal human diploid fibroblasts were arbitrarily chosen for these in-vitro studies. Effects on radiosensitivity were assessed using a conventional colony formation assay. Effects on resistance to the drugs were investigated prospectively (ATP cell viability assay) using 13 fresh tumor samples from consecutive patients operated for ovarian cancer within the context of a Swiss nation-wide randomized prospective clinical trial (SAKK 45/94). RESULTS: Dexamethasone promoted proliferation of 1 of the cell lines without affecting radiosensitivity, while it completely inhibited proliferation of another cell line (effects on radiosensitivity could thus not be examined). Furthermore, dexamethasone induced enhanced radioresistance in 1 of the 8 carcinoma cell lines examined. In the glioblastoma cell line, there was no effect on growth or radioresistance, nor in the fibroblasts. Treatment with dexamethasone enhanced resistance of the malignant cells to carboplatin in 4 of the 13 fresh tumor samples examined, while no enhancement in resistance to paclitaxel was observed. CONCLUSIONS: In agreement with previous reports, we found that dexamethasone may induce radioresistance in human carcinoma cells. Including the published data from the literature, dexamethasone induced enhancement in radioresistance in 4 of 12 carcinoma cell lines (33%), but not in 3 glioblastoma cell lines, nor in 3 fibroblast strains. Dexamethasone also induced enhanced resistance to carboplatin with a similar probability in fresh samples of ovarian cancer evaluated prospectively (in 4 of 13 samples; 31%). We worry that induction of resistance by corticosteroids given to patients undergoing either radiotherapy or chemotherapy with agents causing DNA damage might be associated with a reduced clinical responsiveness in a significant fraction of patients with a carcinoma.     

磁共振功能成像在肝细胞癌中的应用

近年来,肝细胞癌的发病率与死亡率在全球范围内逐年上升。随着分子影像学的发展,磁共振功能成像技术在各系统疾病中的应用越来越广泛,其在肝细胞癌诊断、鉴别诊断、术后疗效评估等方面发挥越来越重要的作用。作者就目前常用的几种功能磁共振成像技术在肝细胞癌中的应用现状进行综述。     

鼻咽癌放射抗拒相关的信号通路

目的 研究具有不同放射抗拒性的人鼻咽癌细胞株CNE-2R与CNE-2的基因表达谱差异,筛选与鼻咽癌放射抗拒相关的基因信号通路.方法 验证已构建的鼻咽癌放射抗拒细胞株CNE-2R的放射抗拒性,选用Human-6v3.0全基因组表达谱微珠芯片,筛选这2种细胞的差异表达基因.对差异基因进行生物信息学分析,寻找与鼻咽癌放射抗拒...     

Targeting the AKT/cyclin D1 pathway to overcome intrinsic and acquired radioresistance of tumors for effective radiotherapy

Purpose: Radiotherapy (RT) is a powerful tool in the treatment of cancer, having the advantage of preserving normal tissues. Clinical outcomes of RT are significantly improved by technological advances, enabling increased radiation doses directed very specifically to a tumor. However, tumor radioresistance remains a major impediment to effective RT. We have shown that human tumor cells surviving after repeated exposure to fractionated radiation (FR) of X-rays for 1 month have acquired radioresistance through constitutive activation of AKT and downstream cyclin D1 nuclear retention. Tumor radioresistance is also proposed to be an intrinsic characteristic of cancer stem cells (CSC), whose efficient DNA repair is thought to confer this phenotype. We have isolated radioresistant CD133-positive cells following exposure to long-term FR. These cells exhibited the CSC phenotype with activation of the AKT/cyclin D1 pathway. In this review, I summarize our current understanding of the molecular mechanisms underlying tumor radioresistance and propose a strategy for overcoming radioresistance by targeting the AKT/cyclin D1 pathway.

Conclusion: Two different mechanisms: acquired radioresistance of surviving tumor cells after RT and intrinsic radioresistance of CSC are associated with tumor radioresistance. Inhibition of the AKT pathway results in radiosensitization of both types of tumor radioresistance.     

环状RNA作为肿瘤标志物及其在肿瘤放疗中应用的研究进展

放疗是肿瘤综合治疗的重要手段之一,但放疗抵抗是影响肿瘤患者放疗疗效及预后的一大难题。由于肿瘤细胞放疗抵抗的机制十分复杂,所以至今还未找到特别有效的调控放疗敏感性的开关分子。环状RNA（circRNA）是一类通过反式剪接使得 3' 末端与 5' 末端共价结合的闭合circRNA分子,具有丰度高、结构稳定和特异性强等特征。circRNA参与肿瘤的发生、发展、侵袭和转移等过程,可以作为新型肿瘤分子标志物和潜在的治疗靶点。此外,circRNA在受照后的肿瘤细胞中存在差异性表达,并可作为微小RNA（miRNA）的海绵,调控与肿瘤放疗抵抗相关的miRNA及其下游信号通路,使其有望成为攻克肿瘤放疗抵抗的突破口。笔者综述了circRNA作为新型肿瘤标志物及其在肿瘤放疗中应用的研究进展。     

Fibrolamellar carcinoma of the liver: radiologic-pathologic correlation.

Fibrolamellar carcinoma is a malignant hepatocellular tumor with distinct clinical and pathologic differences from hepatocellular carcinoma. It differs from hepatocellular carcinoma in demographics, condition of the affected liver, tumor markers, and prognosis. Fibrolamellar carcinoma characteristically manifests as a large hepatic mass in adolescents or young adults (without gender predominance). Cirrhosis; elevated alpha-fetoprotein levels; and typical risk factors for hepatocellular carcinoma such as viral hepatitis, alcohol abuse, and metabolic disease are typically absent. Fibrolamellar carcinoma is characterized pathologically by cords of tumor cells surrounded by abundant collagenous fibrous tissue arranged in a parallel or lamellar distribution. Fibrotic lamellae often coalesce to form a central scar. Fibrolamellar carcinoma characteristically appears on radiologic images as a lobulated heterogeneous mass with a central scar in an otherwise normal liver. Radiologic evidence of cirrhosis, vascular invasion, or multifocal disease--findings typical of hepatocellular carcinoma--is uncommon in fibrolamellar carcinoma. Imaging features of fibrolamellar carcinoma overlap with those of other scar-producing lesions including focal nodular hyperplasia (FNH), hepatocellular adenoma and carcinoma, hemangioma, metastases, and cholangiocarcinoma. FNH, in particular, may simulate fibrolamellar carcinoma, since both have similar demographic and clinical characteristics. Because some believe that radiologic diagnosis of FNH is possible, it is important to understand the imaging appearance of fibrolamellar carcinoma to avoid misdiagnosing this malignant tumor as a FNH.     

食管癌细胞系TE13R120放射抗性与HDAC3、NF-kB和NRAGE关系的研究

目的探讨HDAC3、NF—kB和NRAGE基因与食管癌细胞放射抗性的关系。方法以人食管癌细胞系TE13和由TE13经γ射线反复照射建立的放射抗性细胞系TE13R120为研究对象，用Western blotting技术检测这两种细胞于不同时间、剂量点照射后基因HDAC3、NF—kB和NRAGE的蛋白表达；用流式细胞术检测相同时间、剂量点两种细胞的凋亡和细胞周期分布情况。结果Western blotting显示，与TE13相比，TE13R120细胞照射前后HDAC3的核表达均增高，NF-kB的表达也明显增强，NRAGE在两种细胞胞浆中的表达无差异。与TE13相比，TE13R120中S期细胞明显增多，照射后G2期阻滞明显，凋亡水平较低。结论基因HDAC3和NF-kB可能在食管癌细胞放射抗性形成中发挥作用并可能有协同作用；NRAGE与食管癌辐射抗性的关系有待进一步研究。