经肝动脉灌注化疗并栓塞治疗转移性肝癌的临床疗效

分析了１１８例转移性肝癌经肝动脉插管灌注化疗或并栓塞治疗２２４人次的经验以评价其临床疗效。灌注化疗并碘油乳剂及明胶海绵碎屑栓塞７２例，灌注化疗并碘油乳剂栓塞３２例，单纯灌注化疗１４例。结果显示灌注化疗并碘油乳剂及明胶海绵栓塞者疗效最佳，单纯灌注化疗效果较差。肝内单发转移和多血病变姑息效果最好。本组１，３，５年生存率分别为８６．０％，２５．０％及３．０％。作者认为，经肝动脉插管灌注化疗并栓塞治疗是姑息治疗转移性肝癌的较好方法     

D-二聚体与乳腺癌的关系

作为凝血和纤维蛋白溶解活化的标志物，D-二聚体可快速评估血栓形成活性，并在静脉血栓栓塞症的诊断中发挥重要作用。研究表明在乳腺癌患者的血浆中D-二聚体浓度增加，因此，D-二聚体可以用作乳腺癌高凝状态的标志物。D-二聚体高表达反映了乳腺癌的恶性程度，与乳腺癌的侵袭转移密切相关，但与乳腺癌患者分子分型的关系有待研究。D-二聚体表达水平可以反映乳腺癌患者的身体机能状况，并可以指导构建静脉血栓栓塞症风险分层的风险评估模型。化疗和内分泌治疗会导致部分患者D-二聚体表达升高，在接受化疗前乳腺癌患者的D-二聚体浓度升高与化疗相对剂量强度降低相关。D-二聚体是指导乳腺癌患者抗凝治疗、判断预后的有效生物标志物。     

肺癌患者化疗前后血浆D-二聚体测定的临床意义

目的 :探讨肺癌患者血浆D -二聚体水平与化疗疗效的关系。方法 :采用胶体金方法测定 35例肺癌患者化疗前后血浆D -二聚体的含量。结果 :肺癌患者化疗前血浆D -二聚体水平显著高于正常人 (P <0 0 0 1) ,化疗后有效组 (CR PR)D -二聚体含量显著低于化疗前 (P <0 0 0 1) ,化疗后稳定组D -二聚体含量与化疗前相比 ,差异无显著性 (P <0 0 5) ,化疗后进展组D -二聚体含量明显高于化疗前 (P <0 0 0 1)。结论 :血浆D -二聚体的水平高低可作为肺癌判断预后、观察疗效的一个指标     

合理运用经导管肝动脉化疗栓塞治疗原发性肝癌

迄今为止,手术切除和肝移植仍是肝癌治疗中最彻底的方法。但是,由于肿瘤部位、大小、肝脏储备功能及病人全身情况等的限制,能采用此两种根治方法的病人仍是少数,为此,许多姑息性治疗方法如经导管肝动脉化疗栓塞（TACE）、瘤内酒精注射、微波固化、冷冻治疗、门静脉栓...     

乳腺癌治疗前后血浆D-二聚体水平变化及其临床意义

[目的]探讨乳腺癌患者治疗前后血浆D-二聚体水平变化及其临床意义。[方法]测定95例乳腺癌患者及80例乳腺良性肿瘤患者治疗前后的血浆D-二聚体水平。[结果]治疗前乳腺癌组的血浆D-二聚体水平高于乳腺良性肿瘤组,差异有显著统计学意义（P〈0.01）;治疗前有淋巴结转移乳腺癌患者血浆D-二聚体水平高于无淋巴结转移患者（P〈0.05）,临床Ⅰ~Ⅱ期患者血浆D-二聚体水平低于Ⅲ期患者（P〈0.05）。乳腺癌患者治疗后血浆D-二聚体水平低于治疗前（P〈0.05）。[结论]血浆D-二聚体水平检测在乳腺癌患者的病情评估、疗效观察、预后判断等方面具有重要的临床应用价值。     

经导管肝动脉化疗栓塞在晚期肝癌治疗中的价值

目的 评价经导管肝动脉化疗栓塞在晚期肝癌治疗中的价值。方法 文中对１２例肝癌经股动脉行肝动脉化疗栓塞。结果 半年生存率３３％,达到了改善病人生活质量、延长生存时间的目的。结论 对于晚期肝癌病人,只要一般情况尚可,应积极治疗,但治疗方案要个体化,这样才能在取得较好疗效的同时又不致产生过多的负效应。     

肺癌患者化疗前后血浆D-二聚体和vWF测定的临床意义

目的：探讨肺癌患者血浆D-二聚体和vwF水平与化疗疗效的关系。方法：测定80例肺癌患者化疗前后血浆D-二聚体（免疫比浊法）和vwF（酶联免疫法）的含量。结果：肺癌患者化疗前血浆D-二聚体和vWF水平显著高于正常人（P〈0．01），化疗后有效组血浆D-二聚体和vwF水平明显低于化疗前（P〈0．01）。结论：血浆D-二聚体与vwF水平可作为判断肺癌患者预后及疗效评价的有效指标。     

肺癌患者化疗前后血浆 D-二聚体和 vwF 测定的临床意义

目的：探讨肺癌患者血浆D-二聚体和vwF水平与化疗疗效的关系。方法：测定80例肺癌患者化疗前后血浆D-二聚体（免疫比浊法）和vwF（酶联免疫法）的含量。结果：肺癌患者化疗前血浆D-二聚体和vWF水平显著高于正常人（P〈0．01），化疗后有效组血浆D-二聚体和vwF水平明显低于化疗前（P〈0．01）。结论：血浆D-二聚体与vwF水平可作为判断肺癌患者预后及疗效评价的有效指标。     

经导管肝动脉化疗栓塞在晚期肝癌治疗中的价值

目的　评价经导管肝动脉化疗栓塞在晚期肝癌治疗中的价值。方法　文中对１２ 例肝癌经股动脉行肝动脉化疗栓塞。结果　半年生存率３３％ ,达到了改善病人生活质量、延长生存时间的目的。结论　对于晚期肝癌病人,只要一般情况尚可,应积极治疗,但治疗方案要个体化,这样才能在取得较好疗效的同时又不致产生过多的负效应。     

血浆D-二聚体水平与卵巢癌患者临床特征及化疗预后的关系研究

目的 探讨血浆D-二聚体(D-D)水平与卵巢癌患者临床特征及化疗预后的关系.方法 收集106例卵巢癌患者的临床资料,根据患者血浆D-D水平,将患者分为正常组(≤0.3 mg/L)及升高组(>0.3 mg/L).比较两组患者的临床特征、生存率,分析影响卵巢癌患者化疗预后的危险因素.结果 两组患者FIGO病理分期比较,差异有统计学意义(P﹤0.05);两组患者年龄、组织分化程度、淋巴结转移情况、病理类型及恶性腹腔积液情况比较,差异均无统计学意义(P﹥0.05).升高组患者中位OS及PFS分别为29.7个月(95%CI:27.6~31.8)、9.1个月(95%CI:7.7~10.4);正常组患者中位OS及PFS分别为38.6个月(95%CI:35.8~41.4)、16.1个月(95%CI:13.0~19.2);升高组患者中位OS及PFS明显低于正常组,差异均有统计学意义(Z=13.527、18.461;P﹤0.01).单因素分析结果显示年龄、FIGO病理分期、淋巴结转移、恶性腹腔积液、新辅助化疗、CA125水平、血浆纤维蛋白原、血小板、血浆D-D水平是卵巢癌患者化疗预后的影响因素(P﹤0.01),进一步经Cox回归模型分析结果显示,FIGO病理分期Ⅲ~Ⅳ期、有淋巴结转移、有恶性腹腔积液、无新辅助化疗、血浆D-D水平﹥0.3 mg/L是影响卵巢癌患者化疗生存预后的独立危险因素(P﹤0.01).结论 血浆D-D水平升高是影响卵巢癌患者化疗生存预后的独立危险因素,可作为评估卵巢癌患者化疗生存预后的指标.     

术前FIB-4评分与肝细胞癌术后患者预后的关系研究

  目的   探讨FIB（Fibrosis）-4评分系统与肝细胞癌（HCC）患者临床病理特征及预后的关系。  方法   收集2009年1月至2012年12月间245例接受根治性肝切除手术的HCC患者的临床及随访资料进行分析,利用Kaplan-Meier进行单因素生存分析,Cox比例风险回归模型进行多因素生存分析。  结果   根据患者术前FIB-4评分,将患者分为FIB-4Ⅰ（≤3.25）和FIB-4Ⅱ（ > 3.25）。FIB-4能够预测肝硬化程度（Ishak分级:1~5级 vs. 6级,r=0.681,P < 0.001）,其主要与患者的肝功能指标如谷草转氨酶（P < 0.001）、胆红素（P=0.009）、白蛋白（P=0.001）及血小板计数（P < 0.001）相关,与其他病理特征无关。单因素及多因素分析均表明FIB-4能够预测HCC患者的预后（总生存时间:P=0.037,0.011;无瘤生存时间:P=0.027,0.043）。  结论  FIB-4有可能作为HCC根治性切除术后的预后参考指标之一。      

门脉高压脾机能亢进对根治性治疗肝癌患者预后的影响

  目的  探讨不同程度门脉高压脾机能亢进与脾切除对肝癌患者预后影响。  方法  回顾性分析2008年1月至2018年1月天津市第三中心医院符合米兰标准并行根治性治疗的403例肝细胞肝癌患者临床资料。依据血小板（platelet，PLT）水平、ALBI分级、APRI、血小板/脾长径比值（PSR）等进行Cox比例风险回归分析，对比合并严重脾亢肝癌患者中仅行肝癌根治者与联合脾切除肝癌根治者间临床资料，采用Kaplan-Meier法进行生存分析。  结果  Cox单因素、多因素分析显示，PLT水平是肝癌患者整体生存（overall survival，OS）和无瘤生存（disease free survival，DFS）的独立危险因素。不同血小板水平肝癌患者多因素OS生存曲线具有显著性差异（P=0.013）。PSR、APRI、ALBI分级等肝硬化门脉高压参数也是肝癌预后危险因素。仅行肝癌根治组与联合脾切除肝癌根治组在门脉高压脾亢程度、肝功能分级、肿瘤分期均无显著性差异（P>0.05），生存分析显示，联合脾切除组具有更长的OS（P=0.025），两组1、3、5年生存率分别为100%、98.2%、68.5%和97.1%、79.4%、56.8%。两组DFS比较无显著性差异（P=0.326）。  结论  PLT、PSR、APRI、ALBI等临床参数是合并门脉高压脾亢肝癌患者重要预后影响因素。对合并严重脾亢符合米兰标准的肝癌患者，在肝癌根治同时联合脾切除可提高患者OS。      

HIWI is associated with prognosis in patients with hepatocellular carcinoma after curative resection

BACKGROUND:

PIWI protein family was found to play an important role in stem cell self‐renewal. Overexpression of HIWI, the human homolog of PIWI family proteins, was found in several solid tumors, although the role of HIWI in hepatocellular carcinoma (HCC) and its prognostic value remain unclear.

METHODS:

HIWI expression was measured in stepwise metastatic HCC cell lines (HCCLM3, MHCC97H, MHCC97L, SMMC7721, and HepG2), the normal liver cell line (L02), and HCC tissue samples (n = 20). Proliferation and invasion were investigated in HCC cell lines undergoing HIWI target small interfering RNA transfection. Also explored was HIWI expression in HCC tissue microarrays (n = 168) for survival analysis.

RESULTS:

Levels of HIWI protein and mRNA were up‐regulated in highly metastatic HCC cell lines (HCCLM3, MHCC97H, and MHCC97L), whereas their proliferation and invasion significantly decreased after depletion of HIWI. Intratumoral HIWI expression was higher than that of peritumoral tissue (P < .001) and positively associated with proliferating cell nuclear antigen expression (P < .001). Positive expression of intratumoral HIWI was associated with larger tumor size (P = .047) and intrahepatic metastasis (P = .027) and was an independent risk factor for overall survival (P = .007) and recurrence‐free survival (P = .036), particularly in patients with low serum α‐fetoprotein and low Edmondson‐Steiner grade.

CONCLUSIONS:

HIWI may play a key role in HCC proliferation and metastasis and can be a potential prognostic factor for HCC after curative resection, particularly with well‐differentiated HCC. Cancer 2011. © 2011 American Cancer Society.     

Adjuvant therapy after curative treatment for hepatocellular carcinoma

It is widely accepted that hepatocellular carcinoma (HCC) has an annual recurrence rate of approximately 15-20% even after potentially curative treatment, with the 5-year recurrence rate reaching 80-90%. This recurrence rate is also known to be similar after various curative treatments including resection, percutaneous ethanol injection therapy, and radiofrequency ablation. Generally, in treating patients with HCC associated with hepatitis C or liver cirrhosis, aggressive efforts to prevent secondary carcinogenesis are necessary rather than simply observing the clinical course after treatment. Presently, a combination of peg-interferon and ribavirin is known to be highly effective in patients with difficult-to-treat hepatitis C with a high viral load and genotype I virus. Therefore, indications of these treatments must be considered to prevent secondary carcinogenesis in patients with hepatitis C. Recently, long-term follow-up of low-dose, long-term maintenance therapy using pegylated interferon-α2a for cirrhotic patients clearly showed a preventive effect on HCC occurrence and recurrence. Preventing secondary carcinogenesis by suppressing inflammation employing the same treatment as that against primary carcinogenesis is also important. The molecular targeted agent sorafenib markedly suppresses the serine/threonine kinases of Raf in the MAP kinase cascade and inhibits the tyrosine kinases of angiogenesis factor receptors such as vascular endothelial growth factor and platelet-derived growth factor receptors. It thus simultaneously prevents the proliferation of tumors and inhibits angiogenesis. A clinical trial to examine the recurrence-preventing effect of sorafenib by administration of it after curative treatment such as resection or ablation is in progress (STORM trial: http://clinicaltrials.gov.com, NCT00692770). Treatments to prevent recurrence (including intrahepatic metastasis and multicentric carcinogenesis) as well as early detection and early curative treatment are extremely important to improve the prognosis of patients with HCC. Thus, further research on this issue should be carried out, especially in relation to molecular targeted therapy.     

The prognosis of hepatocellular carcinoma after curative hepatectomy in young patients

Age at diagnosis is a reported prognostic factor in a variety of solid cancers. In hepatocellular carcinomas (HCCs), several previous studies focused on patient age, but demonstrated inconclusive results on prognosis of young patients. Clinical outcome may differ according to the balance between tumor''s own biologic behavior and underlying liver function thus explaining the inconclusive results in previous studies. In this study, we enrolled 282 patients who underwent curative hepatectomy for primary HCCs and had Child Pugh Class A, representing good liver function. Clinicopathologic features were compared between patients aged ≤40 years (young age group) and those aged >40 years (old age group). Thirty-five patients (12.4%) were classified as the young age group and showed larger tumor size (>5cm), higher Edmondson grade, more frequent intrahepatic metastasis and higher alpha-fetoprotein level (>200ng/mL) than old age group. Young age group showed shorter disease specific survival than the old age group. Symptomatic presentation without surveillance was more frequent in the young age group than old age group (45.7% vs. 23.9%). In gene expression profiling analysis, 69 differentially expressed genes between young and old age groups were generated and these genes were mostly associated with cell cycle or cell division. Mitotic rate was significantly higher in HCCs of young patients than those of old patients. In conclusion, HCCs in young patients have distinct clinicopathologic features. Poor prognosis in the young age group could be explained by late detection as well as their own aggressive tumor biology.     

Upregulation of vasohibin-1 expression with angiogenesis and poor prognosis of hepatocellular carcinoma after curative surgery

Vasohibin-1 has recently been found and is known as an endogenous angiogenesis inhibitor, but the role of vasohibin-1 in hepatocellular carcinoma (HCC) is unknown. This study investigated the expression pattern of vasohibin-1, its correlation with clinicopathological features, and its potential role in tumor angiogenesis and prognosis of HCC. Expression of vasohibin-1, vascular endothelial growth factor-A (VEGF-A), and intratumoral microvessel density (MVD, labeled by CD34) were assessed by immunohistochemistry in 117 HCC specimens and adjacent nontumor liver tissues (ANLT). Correlation between vasohibin-1 and VEGF-A, MVD, and clinicopathological features was then investigated. Prognostic value of these factors was determined using Kaplan-Meier analysis and a Cox proportional hazards regression model. Cytoplasm high expression of vasohibin-1 was detected in 38.5% (45/117) of the HCC tissues, which was significantly higher than that in 16.2% (19/117) of ANLT (P?相似文献   

磁共振弥散加权成像评价肝癌冷冻术后近期疗效

目的:探讨采用磁共振弥散加权成像(MRI-DWI)对鉴别肝细胞性肝癌(HCC)冷冻术后肿瘤坏死、残留的应用价值.方法:对接受冷冻治疗的27例肝癌患者共30个病灶行T1 WI、T2WI常规MRI平扫、DWI序列及动态增强扫描.观察肿瘤冷冻前、后MRI信号改变.对HCC一般特征与ADC值的相关性进行分析.比较冷冻前后正常肝脏、肿瘤组织及术后坏死、残留组织的ADC值.结果:冷冻坏死的肝肿瘤组织在T1WI图中呈稍低或稍高信号,T2WI呈低或等信号,DWI呈低信号,动态增强无强化.活性残留肿瘤14个(其中12个肿瘤直径＞5.0 cm),残留率为46.7％.b值=800 s/mm2时,ADC值由低到高依次为:术后残留肿瘤组织(0.98±0.17)×10-3 mm2/s、术前肝肿瘤组织(1.03±0.20)×10-3 mm2/s、正常肝组织(1.14 ±0.07)×10-3mm2/s、术后坏死肿瘤组织(2.07±0.23)×10-3 mm2/s.肝肿瘤组织与对照组正常肝组织ADC值相比,差异有统计学意义(P=0.016).肝肿瘤组织ADC值与肿瘤大小不相关(r=-0.10,P=0.614),与直径范围,肿瘤分期、是否远端转移无关(P＞0.05)、与分化程度有关(P＜0.05).肿瘤坏死区ADC值与术前肿瘤组织相比,差异均有显著统计学意义(P＜0.01).残留组织ADC值与坏死组织及正常肝组织相比,差异均有统计学差异(P＜0.01,P=0.03),与肿瘤组织相比无统计学差异(P=0.192).结论:MRI-DWI能有效鉴别肝癌冷冻术后的病灶坏死及残留,为进一步的临床诊治提供影像学依据.     

High expression of AP-4 predicts poor prognosis for hepatocellular carcinoma after curative hepatectomy

The aim of this study was to evaluate the association between activating enhancer binding protein 4 (AP-4) tissue expression and patient prognosis in hepatocellular carcinoma (HCC). The levels of AP-4 mRNA and protein in tumor and para-tumor tissue were evaluated in 30 HCC cases by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot. Additionally, AP-4 protein expression in 112 HCC was analyzed by immunohistochemistry. The correlation of AP-4 expression and patients’ clinicopathological parameters was evaluated. Survival analysis was performed using the Kaplan–Meier method and Cox’s proportional hazards model. By RT-PCR and Western blot, the levels of AP-4 mRNA and protein were significantly higher in HCC, compared to that in para-tumor tissue (p?<?0.001). Immunohistochemical staining revealed that AP-4 was highly expressed in 53.6 % of the HCC patients. The AP-4 expression level was closely associated with serum alpha fetoprotein elevation, tumor size, histological differentiation, tumor recurrence, tumor metastasis, and tumor stage. Kaplan–Meier survival analysis showed that a high expression level of AP-4 resulted in a significantly poor prognosis of HCC patients. Multivariate analysis revealed that AP-4 expression level was an independent prognostic parameter for the overall survival rate of HCC patients. These findings provide evidence that a high expression level of AP-4 serves as a biomarker for poor prognosis for HCC. Thus, we speculate that AP-4 may be a potential target of antiangiogenic therapy for HCC.     

Prediction of microvascular invasion before curative resection of hepatocellular carcinoma

BACKGROUND: The accurate staging of hepatocellular carcinoma (HCC) is important in establishing treatment strategies and prognosis. Among tumor factors, microvascular invasion, one of TNM staging components and prognostic factors, is underestimated preoperatively, due to inaccuracy of imaging modalities. We investigated preoperative predictors of microvascular invasion. METHODS: We reviewed 190 consecutive HCC patients given curative resection from 1999 to 2006. All were treatment-naive and monitored every 3 months after resection. Tumor recurrence, survivals, and clinicopathological factors associated with microvascular invasion were analyzed. RESULTS: The 5-year disease-free survival (DFS) rate was 39.4%(median follow-up duration: 35 months). On resection pathology, 38.9% (74/190 patients) had microvascular invasion undetected preoperatively, using liver spiral computed tomography (CT) or angiography. Independent predictors of microvascular invasion were tumor size (P = 0.043), number (P = 0.011), and Edmondson grade (P = 0.001). Patients with Edmondson grade 1 and size <5 cm had no microvascular invasion, while those with grade > or =2 had higher incidences (7/18 patients, 38.8%) even in small tumor (<2 cm). When tumors recurred, presence of microvascular invasion independently increased incidences of multiple tumors, portal vein invasion, and diffuse-infiltrative patterns significantly. CONCLUSIONS: Preoperative predictors of microvascular invasion are tumor size, number, and Edmondson grade, which may be useful for making clinical decisions in both non-surgical and surgical candidates.