基于肝细胞癌临床数据预测淋巴结转移列线图的构建

目的 :利用肝细胞癌(HCC)患者临床数据构建预测淋巴结转移危险因素的Nomogram模型。方法 :收集恩施土家族苗族自治州中心医院2016—2021年收治的328例HCC患者临床数据,将50例淋巴结转移患者纳入转移组,余278例纳入对照组。多因素Logistic回归分析寻找淋巴结转移的风险因素,在此基础上构建Nomogram模型。结果 :甲胎蛋白(>243.35μg/L)、γ-谷氨酰基转移酶(>181.82 U/L)、肿瘤最大直径(>6.17 mm)、肿瘤个数(>1个)是HCC患者淋巴结转移的危险因素(均P<0.05)。Nomogram模型被成功构建,内部验证结果显示预测HCC患者淋巴结转移C-index为0.805(95%CI为0.086～1.325),风险阈值>0.058,且临床净收益均高于甲胎蛋白、γ-谷氨酰基转移酶、肿瘤直径、肿瘤个数。结论 :基于HCC临床数据成功构建了预测淋巴结转移的Nomogram模型,该模型对于临床筛查预判HCC患者可能出现淋巴结转移具有实用价值。     

肝细胞癌门静脉癌栓的研究进展

肝内复发和转移是肝细胞癌治疗困难和死亡的主要原因。门静脉检在复发和转移过程中起关键作用。Q     

肝细胞癌合并门静脉癌栓外科治疗的疗效观察

目的探讨肝细胞癌合并门静脉癌栓（PVTT）外科治疗的效果。方法对156例肝细胞癌合并门静脉主干或第一分支癌栓的患者,均行肝癌联同门静脉癌栓切除或取栓,其中94例患者术后行肝动脉和（或）门静脉化疗。结果术后3例死于肝功能衰竭,2例死于术后并发症,余术后恢复良好,术后1、3、5年生存率分别为58．1％（86/148）、18．9％（28／148）、5．4％（8／148）。结论肝切除和门静脉切开取栓术是肝细胞癌合并PVTT的有效治疗方法,术后联合肝动脉和（或）门静脉化疗能提高治疗效果,延长患者的生存期。     

肝细胞癌门静脉癌栓形成机制

原发性肝细胞癌(hepatocellular carcinoma,HCC;简称肝癌)是世界上常见的恶性肿瘤之一,在我国已成为第2位的癌症杀手.肝癌起病隐匿,大部分患者诊断时已属晚期,预后很差,总体5年生存率仍不超过7%.肝癌侵犯门静脉形成门静脉癌栓(portal vein tumor thrombus,PVTT)并导致肝内播散是其主要原因之一.     

肝细胞癌合并门静脉癌栓的外科治疗

近年来 ,肝细胞癌 (HCC)患者生存率已有所提高 ,但 HCC肝内复发和转移率仍高 ,总的预后较差 [1 ] 。因为 HCC常侵犯门静脉形成门静脉癌栓 (portaltumor thrombus,PTT) ,癌栓通过门静脉血流向肝内播散 ,导致肝内播散和复发。我们对 HCC合并 PTT采取肝切除和门静脉切开取癌栓术 ,部分患者术后联合门静脉化疗 ,取得了满意效果 ,现报道如下。1　资料与方法1.1　一般资料　 1996年 1月 - 2 0 0 1年12月我院共行 HCC手术切除 35 0例 ,其中合并门静脉癌栓 4 7例 (占 13.4 % ) ,其中男性 4 0例 ,女性 7例 ,年龄 16岁～ 6 7岁 ,平均 4 5 .8…     

肝细胞癌癌栓形成机制及治疗——肝细胞癌门静脉癌栓形成机制

原发性肝细胞癌（hepatocellular carcinoma,HCC;简称肝癌）是世界上常见的恶性肿瘤之一,在我国已成为第2位的癌症杀手。肝癌起病隐匿,大部分患者诊断时已属晚期,预后很差,总体5年生存率仍不超过7％。     

肝细胞癌伴门静脉癌栓不同治疗方法的比较

目的 比较肝细胞癌合并门静脉癌栓(ｔｕｍｏｒ ｔｈｒｏｍｂｉ ｉｎ ｐｏｒｔａｌ ｖｅｉｎ,ＰＶＴＴ）不同治疗方法的疗效及其意义。方法 １４７例肝细胞癌伴门静脉主干或第１分支癌栓的住院患者,按不同治疗方法分成４组：保守治疗组（Ａ组,１８例）;肝动脉结扎和（或）肝动脉插管化疗组（Ｂ组,１８例）,术后定期栓塞化疗;肝癌联同ＰＶＴＴ切除组（Ｃ组,７９例）;手术切除＋肝动脉化疗栓塞和（或）肝动脉置管或门静脉     

肝细胞癌伴门静脉癌栓的治疗进展

肝细胞癌是我国常见的恶性肿瘤之一,门静脉癌栓的出现则表明肝癌已近中晚期,预后很差。随着对门静脉癌栓的认识以及治疗方法的改进,肝癌伴门静脉癌栓患者的临床疗效有了较大幅度的提高。本文就近年来临床上关于肝癌伴门静脉癌栓的治疗进展作一综述。     

肝细胞癌伴门静脉癌栓的诊治现状及展望

0 引言 肝细胞癌(hepatocellular carcinoma,HCC)是最常见的恶性肿瘤之一,由于起病隐匿,病情进展快,发现时多属中晚期,且40.0％～90.2％晚期HCC患者伴门静脉癌栓(portal vein tumor thrombus,PVTT)形成[1].Chau等[2]报道手术切除标本中直径＜2 cm的HCC镜下PVTT发生率为40.5％;而直径为2.1～4.0 cm的HCC伴PVTT发生率高达49.6％,故小肝癌患者门静脉内形成癌栓的比例也非常高.PVTT是HCC肝内复发及转移的重要原因,严重限制了手术切除和介入等治疗的使用,成为近几年肝癌研究的难点与热点.同时,PVTT又能够引起或加重门静脉高压症,患者往往在数月内死亡,预后极差.所以,对HCC伴PVTT进行积极有效的诊治,是提高HCC患者生存率和生活质量的重要途径.     

原发性肝癌合并门静脉癌栓的治疗

原发性肝癌(HCC)合并门静脉癌栓(PVTT)是肝癌治疗的难点之一.目前临床上对HCC合并PVTT有多种治疗方法,对延长肝癌患者的生存时间和提高生存质量都具有重要意义,手术治疗和介入治疗在其中发挥着重要的作用.     

原发性肝癌并发门静脉癌栓的治疗策略

 门静脉癌栓是原发性肝癌的常见并发症,一旦发生,常预示着病情已处晚期,难以逆转,预后极差。文章介绍了门静脉癌栓现有的治疗方法,提倡多学科综合治疗,提高晚期肝癌患者的生存期。     

原发性肝细胞癌合并门静脉癌栓的研究进展

门静脉癌栓（portal vein tumor thrombus,PVTT）是影响原发性肝细胞癌治疗策略及预后的重要因素。近年与PVTT相关的分子信号通路不断被发现,但PVVT形成机制及其研究和临床诊疗仍面临较大挑战。本文就原发性肝细胞癌合并PVTT的研究进展作一综述。     

Proton beam therapy for hepatocellular carcinoma with portal vein tumor thrombus

BACKGROUND: Treatment modalities for patients with hepatocellular carcinoma (HCC) who have portal vein tumor thrombus (PVTT) are limited and controversial; furthermore, the prognosis for these patients is extremely poor. The authors conducted a retrospective review to determine the role of proton beam therapy in the treatment of patients who had HCC with PVTT. METHODS: Twelve patients with HCC who had tumor thrombus in the main trunk or major branches of the portal vein (clinical T3-T4N0M0) were treated with proton beam therapy. At the time they received proton beam irradiation, patients ranged in age from 42 years to 80 years (median, 62 years), and their tumors ranged in size from 40 mm to 110 mm (median, 60 mm) in greatest dimension. A total dose of 50-72 gray (Gy) (median, 55 Gy) in 10-22 fractions was delivered to the tumors, including PVTT. RESULTS: All tumors that were treated with proton beam therapy remained controlled at a median follow-up of 2.3 years (range, 0.3-7.3 years). Among 12 patients, 10 patients had new liver tumors outside the irradiated volume 0.1-2.4 years after proton beam therapy, and 3 patients also had distant metastases; consequently, 8 patients died of disease, and 2 patients were salvaged by further therapies. The remaining two patients were alive with no evidence of disease 4.3 years and 6.4 years after proton beam therapy. The progression-free survival rates were 67% at 2 years and 24% at 5 years. The median progression-free survival was 2.3 years. According to the Acute Radiation Morbidity Scoring Criteria (Radiation Therapy Oncology Group), therapy-related toxicity > or = Grade 3 was not observed. CONCLUSIONS: Proton beam therapy for patients with HCC who had PVTT was feasible and effective. It appeared to improve survival and local control significantly for these patients.     

肝细胞癌合并门静脉癌栓的治疗进展

门静脉癌栓是中晚期肝癌患者最常见的并发症之一,已成为影响肝癌患者术后复发转移和总体生存预后的主要因素之一。近年来,随着医疗技术的不断发展,肝癌精准治疗和多学科协作诊疗等理念不断深入,除传统的手术治疗外,局部消融术、靶向药物治疗、肝动脉栓塞化疗、三维适形放疗等多种手段的联合应用,经过临床应用证实疗效更加显著,肝癌合并门静脉癌栓的综合治疗理念已贯穿始终。本文就肝细胞癌伴门静脉癌栓的最新治疗进展做一综述,以供临床参考。     

外科手术治疗肝癌合并门静脉癌栓的疗效分析

目的 探讨肝细胞癌（HCC）合并门静脉癌栓（PVTT）患者行外科手术治疗的疗效。方法 收集1998年1月至2008年12月34例经手术治疗的HCC合并PVTT患者的临床诊治资料并进行回顾性分析。结果 34例HCC合并PVTT患者术后1个月内死亡2例,32例恢复良好。获随访29例（90.6％）,中位生存时间为16.2个月,1、2、3、4、5年生存率分别为51.7％、37.9％、24.1％、10.3％和3.4％。其中术后行门静脉及肝动脉双置管灌注化疗者23例,1、2、3、4、5年的生存率分别为57.1％、42.9％、28.6％、14.3％和4.7％,中位生存时间为19.6个月;单纯手术组9例,1、2、3、4、5年的生存率分别为45.0％、22.2％、11.1％、0、0,中位生存时间为13.5个月。两组生存率比较,差异有统计学意义（P＜0.05）。结论 肝切除加PVTT摘除术是治疗HCC合并PVTT有效的方法之一,术后门静脉和肝动脉双置管灌注化疗能提高患者远期生存率。     

Independent factors and predictive score for extrahepatic metastasis of hepatocellular carcinoma following curative hepatectomy

Background.

Postoperative extrahepatic metastasis (EHM) contributes to a poor prognosis in patients with hepatocellular carcinoma (HCC) after hepatectomy. This study was aimed to develop a practical method that can be used to predict postoperative EHM.

Methods.

In total, 578 patients were enrolled. We analyzed the clinicopathological features of the tumors and did a long-term follow-up to observe HCC recurrence. Postoperative EHM was detected in 136 patients, and multivariate analysis was used to confirm independent risk factors for postoperative EHM. After the factors were identified, a predictive scoring system was constructed as a weighted sum of these factors. The cutoff value that determines a high risk for EHM was defined by maximizing the Youden''s index of the receiver operating characteristic curve.

Results.

Microvascular invasion, incomplete capsule, and larger tumor diameter were the three independent factors predictive for a high risk for EHM. The scoring system was derived with an area under the curve (AUC) of 0.81 for postoperative 10-year EHM prediction. A cutoff value of 43 was derived and validated with a sensitivity >90% and specificity >60% to predict the development of EHM. This system was further verified in a subgroup of Barcelona Clinic Liver Cancer stage 0–A patients with an AUC of 0.82. When the cutoff value was set at 43, the sensitivity and specificity were 90.38% and 64.88%, respectively.

Conclusions.

Our predictive scoring system may be used to identify HCC patients who have a high risk for EHM following curative hepatectomy.     

HCC伴PVTT经肝动脉-门静脉联合化疗栓塞疗效观察

目的对原发性肝癌(HCC)伴门静脉癌栓(PVTT)的患者行肝动脉-门静脉联合化疗栓塞治疗后1年内的疗效进行观察。方法 选择符合纳入标准的HCC伴PVTT患者124例进行肝动脉-门静脉联合化疗栓塞治疗,观察治疗后在肿瘤及门脉癌栓变化、AFP变化、生存质量及生存率方面随访其1年内的疗效。结果 AFP变化,介入后转阴率为27.4%。治疗后肿瘤及门静脉癌栓变化,CR 6例(4.8%),PR 39例(31.5%),NC 45例(36.3%),PD 34例(27.4%)。治疗后1月、3月生存质量较前提高,两者比较差异有统计学意义(P<0.01),治疗后1年较前降低,两者比较差异有统计学意义(P<0.01)。生存率方面,治疗后1月、3月、6月和1年生存率分别100.0%、89.1%、71.6%和58.3%。结论 肝动脉-门静脉联合化疗栓塞治疗HCC伴PVTT患者改善生存质量、提高生存率方面均有较明显的短期疗效。     

Correlation of four vascular specific growth factors with carcinogenesis and portal vein tumor thrombus formation in human hepatocellular carcinoma

The aim of the present study was to detect the correlation between the expression of vascular endothelial growth factor (VEGF), angiopoietin 2 (Ang2), ephrinB2 and endocrine gland-derived vascular endothelial growth factor (EG-VEGF) and carcinogenesis or portal vein tumor thrombus (PVTT) formation in human hepatocellular carcinoma (HCC). The expression of VEGF, Ang2, ephrinB2 and EG-VEGF was detected by RT-PCR in 54 cases HCC without PVTT (group A), 9 cases HCC with PVTT (group B), 10 normal liver tissues (group D) and 10 cirrhosis tissues (group C). The samples were also stained with CD34 by immunohistochemistry. Quantitation of microvessel density (MVD) and semi-quantitation of VEGF, Ang2, ephrinB2 and EG-VEGF expression were analyzed to find the relations. The MVD was 146.69 +/- 77.79, 214.07 +/- 54.41, 32.85 +/- 8.49 and 34.83 +/- 8.29 in group A-D respectively with significant difference (F = 19.77, P = 0.000). The MVD in group A was higher than that in group C P = 0.006, but lower than that in group B P < or = 0.05 or 0.01. The expression levels of VEGF165, VEGF189, Ang2 and EG-VEGF mRNA were significantly different among the groups. The expression levels of VEGF165, Ang2 and EG-VEGF mRNA in group A were all higher than those in group C, but lower than those in group B P < 0.05 or 0.01. The MVD was significantly correlated with VEGF165, VEGF189, Ang2 and EG-VEGF mRNA with Spearman's related coefficient being 0.764, 0.510, 0.640 and 0.366 in HCC (P = 0.000, 0.000 0.000 and 0.003). In conclusion VEGF, Ang2 and EG-VEGF mRNA may play a role in angiogenesis and carcinogenesis of HCC. They can promote PVTT formation in HCC by modulating angiogenesis.