Cuproptosis is a novel form of programmed cell death characterized by the accumulation of copper ions in the mitochondria, the formation of DLAT oligomers, and the depletion of Fe-S cluster proteins. However, the alterations in mitochondrial morphology and function during cuproptosis and the potential role of mitophagy in cuproptosis remain insufficiently elucidated. In this study, we induced cuproptosis of breast cancer cells using Elesclomol (ES) and assessed changes in mitochondrial reactive oxygen species, mitochondrial membrane potential, and oxygen consumption rate. Stable cell lines with overexpression or knockdown of PINK1/Parkin genes were constructed to elucidate the impact of mitophagy on cuproptosis. Subcutaneous mouse xenograft models were employed to identify drugs that may synergize with ES and enhance antitumor effects. Our results demonstrated that ES induced cuproptosis of breast cancer cells, which was associated with the activation of PINK1/Parkin-mediated mitophagy. Both gene knockdown and pharmacological inhibition of mitophagy enhanced the sensitivity of breast cancer cells to cuproptosis in vitro and in vivo. The combination of dichloroacetate (DCA) and ES exhibited a synergistic antitumor effect without significant tissue damage on the brain, heart, liver, and kidneys in subcutaneous mouse xenograft models. Collectively, our findings reveal that inhibiting PINK1/Parkin-mediated mitophagy enhances the sensitivity of breast cancer to cuproptosis, offering a novel combined treatment strategy for breast cancer.

Aims: Oxidative stress reflected by elevated reactive oxygen species (ROS) in the tumor ecosystem, is a hallmark of human cancers. The mechanisms by which oxidative stress regulate the metastatic ecosystem and resistance remain elusive. This study aimed to dissect the oxidative stress-sensing machinery during the evolvement of early dissemination and acquired drug resistance in breast cancer. Methods: Here, we constructed single-cell landscape of primary breast tumors and metastatic lymph nodes, and focused on RGS5(+ )endothelial cell subpopulation in breast cancer metastasis and resistance. Results: We reported on RGS5 as a master in endothelial cells sensing oxidative stress. RGS5(+ )endothelial cells facilitated tumor-endothelial adhesion and transendothelial migration of breast cancer cells. Antioxidant suppressed oxidative stress-induced RGS5 expression in endothelial cells, and prevented adhesion and trans- endothelial migration of cancer cells. RGS5-overexpressed HLECs displayed attenuated glycolysis and oxidative phosphorylation. Drug-resistant HLECs with RGS5 overexpression conferred acquired drug resistance of breast cancer cells. Importantly, genetic knockdown of RGS5 prevented tumor growth and lymph node metastasis. Conclusions: Our work demonstrates that RGS5 in lymphatic endothelial cells senses oxidative stress to promote breast cancer lymph node metastasis and resistance, providing a novel insight into a potentially targetable oxidative stress-sensing machinery in breast cancer treatment.

目的：利用Gail模型，对超声发现乳腺肿物且BI-RADS4类患者是否活检做出建议，提高早期诊断精准度及治疗效率。方法：收集乳腺超声诊断为BI-RADS4类并行麦默通活检的461例患者5年前Gail模型的指标（包括年龄、初潮年龄、初产年龄、乳腺活检次数及乳腺病史），一级家属史、种族及病理诊断，计算5年发病风险，绘制ROC曲线，计算曲线下面积，重新定义最佳界值并分为高风险组和低风险组，比较两组在BI-RADS4（a、b、c）类患者中的预测准确率。结果：Gail模型以1.67%为界值预测5年发病风险准确率较低

目的:探讨KIF23在三阴性乳腺癌(TNBC)细胞中的表达及其对TNBC细胞增殖、迁移和侵袭的影响.方法:采用实时荧光定量PCR(qPCR)法检测KIF23mRNA在正常乳腺细胞(MCF-10A)和TNBC细胞(MDA-MB-231、MDA-MB-468、MDA-MB-436)中的表达.选取KIF23表达量最高的细胞,分为KIF23小干扰RNA(si-KIF23)组、阴性对照(NC)组和空白组,NC组和si-KIF23组,分别用siRNA-NC和KIF23siRNA进行细胞转染,空白组不做处理.分别采用qPCR和Western blotting法检测细胞KIF23mRNA和蛋白表达.CCK-8法检测细胞增殖能力,Transwell实验检测细胞侵袭和迁移能力.结果:与正常乳腺细胞MCF-10A比较,KIF23在3种TNBC细胞中的表达均明显上调(均P＜0.05),且在MDA-MB-231细胞中的表达量最高.与空白组及NC组比较,si-KIF23组KIF23mRNA和蛋白表达量均显著降低,细胞增殖、侵袭和迁移能力明显降低(均P＜0.05).结论:KIF23在MDA-MB-231、MDA-MB-468、MDA-MB-436细胞中高表达;沉默KIF23基因能降低MDA-MB-231细胞的增殖、迁移和侵袭能力.

目的 比较麦默通活检(MMT)与空芯针穿刺活检(CNB)在乳腺癌中的诊断价值.方法 选择经手术病理确诊的乳腺癌患者1008例,其中术前行MMT者509例、CNB者499例;以手术病理结果 为标准,分析CNB和MMT诊断乳腺癌的价值;从1008例患者中选取活检前已行乳腺钼靶检查者190例,其中CNB 119例、MMT 71例,分析组织学低估与乳腺钼靶钙化的关系.结果CNB取样失败率4.8％,而MMT无取样失败者(P<0.01);CNB与术后病理诊断符合率为94.1％,低于MMT的98.2％(P<0.01);CNB诊断假阴性率0.6％,而MMT无诊断假阴性者(P>0.05);CNB组织学低估率5.3％,高于MMT的1.8％(P<0.01);乳腺癌病灶直径≤2 cm、>2～5 cm时MMT诊断符合率高于CNB(P均<0.05),>5 cm时CNB与MMT诊断符合率差异无统计学意义.相关分析显示,CNB组织学低估与乳腺钼靶钙化存在正相关(r=0.193,P<0.05),MMT组织学低估与乳腺钼靶钙化无明显相关性(r=-0.003,P>0.05).结论 MMT在乳腺癌诊断准确性方面优于CNB,尤其是在直径≤5 cm的病灶中;CNB较MMT更易发生组织学低估和活检取样失败,CNB的组织学低估可能与乳腺病灶内钙化有关.

Background: Emerging studies have demonstrated that circular RNAs (circRNAs) are key regulators for tumorigenesis in cancers, including papillary thyroid carcinoma (PTC). In this study, we aimed to explore the effects of circ_LDLR on PTC. Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to determine the levels of circ_LDLR, miR-195-5p and lipase H (LIPH). RNase R digestion assay and Actinomycin D assay were utilized to analyze the characteristics of circ_LDLR. Colony formation assay and 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) assay were conducted to evaluate cell proliferation. Western blot assay was used for the determination of protein levels. Flow cytometry analysis was applied to determine cell apoptosis. Transwell assay was performed to determine cell migration and invasion. Dual-luciferase reporter assay was used to verify the associations among circ_LDLR, miR-195-5p and LIPH. The murine xenograft model was constructed to explore the roles of circ_LDLR in vivo. Results: Compared to normal tissues and cells, circ_LDLR was upregulated in PTC tissues and cells. Silencing of circ_LDLR suppressed PTC cell colony formation, proliferation, migration and invasion and promoted apoptosis in vitro and hampered tumor growth in vivo. For mechanism investigation, circ_LDLR could regulate LIPH expression via sponging miR-195-5p. Moreover, miR-195-5p inhibition restored the effects of circ_LDLR knockdown on the malignant behaviors of PTC cells. MiR-195-5p overexpression inhibited PTC cell colony formation, proliferation, migration and invasion and facilitated apoptosis by targeting LIPH. Conclusion: Circ_LDLR knockdown decelerated PTC progression by regulating miR-195-5p/LIPH axis, which might provide a novel therapeutic target for PTC.

BACKGROUND:This study aims to determine the incidence of N2- or N3-stage disease in a cohort of patients with T1-T2 invasive breast cancer and one or two positive sentinel lymph nodes (SLNs), and identify the risk factors for N2/3 disease in this cohort.METHODS:The present study involved 298 patients with T1-T2 tumors who underwent SLN biopsy and were found to have one or two metastatic SLNs. The proportion of patients with N2/3 disease was calculated in the whole cohort, and in the T1 and T2 subgroups. Furthermore, univariate and multivariate analyses were used to identify the risk factors for N2/3 disease in the cohort.RESULTS:The final N stage, as determined by the postoperative pathological examination, was N1 for 250 (83.9%) patients, and N2 or N3 for 48 (16.1%) patients (11.41% had clinical N2 disease, while 4.70% had clinical N3 disease). Among the 156 patients with T1 tumors, 17 (10.9%) patients had N2/3 disease, while for the 142 patients with T2 tumors, 31 (21.8%) patients had N2/3 disease. T2 stage, lymphovascular invasion, and the number of positive SLNs were independent predictors of N2/3 disease in the cohort (P<0.05).CONCLUSIONS:N2/3 lymph node metastasis occurs in patients with T1-T2 breast cancer, and one or two positive SLNs, particularly in patients with T2 tumors. The rate of N2/3 disease is not negligible. T2 stage, lymphovascular invasion, and the number of positive SLNs were independent predictors of N2/3 disease in the present patient population.

This study aimed to evaluate the impacts of 21-gene recurrence score (RS) and St. Gallen International Expert Consensus on treatment decision and prognosis of patients with invasive breast cancer. We retrospectively analyzed the therapy protocol and outcome of 134 cases based on age, body mass index (BMI), menopause, pathological types, tumor-node-metastasis (TNM) stages, percentage of estrogen receptor (ER), progesterone receptor (PR), human epidermal growth factor 2 (HER2), Ki-67, molecular subtype, and tumor biomarkers. RS was calculated based on 21-gene assay following traditional (old RS cutoff) and updated (new RS cutoff) National Comprehensive Cancer Network (NCCN) guideline. In addition, we also compared treatment protocol of NCCN guidelines with St. Gallen International Expert Consensus. The results showed that BMI, PR, Ki-67, and molecular subtype are critical for the evaluation of risk factors. Based on the new cutoff, low, middle, and high RS were 18%, 66%, and 16%, respectively. In contrast, based on the old cutoff, low, middle, and high RS were 60%, 29%, and 11%, respectively. The agreement rate of NCCN guidelines and St. Gallen International Expert Consensus for adjuvant treatment was 50. However, there is minimal agreement (0.151, 0.071) in kappa coefficient of old and new cutoff. This study revealed that the combination of NCCN guidelines and St. Gallen International Expert Consensus might improve the benefits of adjuvant treatment in patients with early invasive breast cancer.

Background: This study investigated the diagnostic and prognostic values of kinesin superfamily proteins (KIFs) in breast cancer (BC) patients. Material/Methods: All data were obtained from the Cancer Genome Atlas. DESeq was run to test for differentially expressed KIF genes. Patients were divided into high- and low-expression groups according to the median expression values of each KIF genes. Survival data were calculated using the Cox proportional hazard model. Comprehensive survival analysis was performed to evaluate the prognostic value of the prognostic signature. Gene set enrichment analysis (GSEA) was conducted to identify associated gene ontology and KEGG pathways. Results: Bioinformatics analysis showed that all KIF genes were significantly enriched during DNA replication and the cell cycle, and co-expressed with each other. Thirteen KIF genes were differentially expressed in cancer and adjacent tissues, and high levels of KIF15, KIF20A, KIF23, KIF2C and KIF4A genes were significantly correlated with poor overall survival (OS). GSEA showed that BC patients with high expression of KIF15, KIF20A, KIF23, KIF2C and KIF4A were enriched in the cell cycle process, P53 regulation pathway and mismatch repair. Combinations of low expression of KIF15, KIF20A, KIF23, KIF2C and KIF4A were more highly correlated with favorable OS. Nomograms showed that the KIF4A risk score provided the maximum number of risk points (range 0-100), whereas other genes made a lower contribution. Conclusions: We conclude that 13 KIF genes are differentially expressed in BC tumor tissues, and KIF15, KIF20A, KIF23, KIF2C and KIF4A are associated with prognostic factors in BC.

Background: Base on the "seed and soil" theory, the presence of circulating tumor cells (CTC) in breast cancer has been suggested to be the active source of metastatic spread in primary tumors. During metastasis formation, epithelial cells undergo massive changes in their characteristics and increase their motility in order to migrate, a process termed epithelial-to-mesenchymal transition (EMT). Here, we applied a quantifiable, dual-colorimetric RNA-in situ hybridization assay in exploring whether CTC or its subtypes in peripheral blood could be suitable biomarkers in early breast cancer. Methods: A total of 5 ml of blood was analyzed for CTC with the CanPatrolTM system (SurExam, Guangzhou, China) for the detection and classification of CTCs. Results: CTCs consist of different epithelial and mesenchymal compositions were observed in 115/142 (81.0%) patients. Sixty-seven of 142 patients investigated were positive for lymph nodes, and 52.8% (75/142) were negative, respectively. The presence of CTC at baseline was correlated to lymph node metastases (P=0.042), but no association was found with tumor size, grading, histological types, hormone receptor status or molecular subtypes. Strikingly, nodal involvement is positively correlated with the exclusively epithelial marker positive CTC (defined as EpCAM+ and/or CK8+ and/or CK18+ and/or CK19+ by a multi-marker probe, P=0.010). Conclusions: Our finding suggest that CTC and its subpopulations were observed visually by the currently used detection methods and evaluation of CTCs in early stage breast cancer patients provides potential clinical information. A subset of CTCs in patients with early BC shows EMT and the clinical relevance on the prognosis of CTCs has to be further validated in a prospective trial.

BACKGROUNDGastrectomy remains the primary therapeutic method for resectable gastric cancer. Thought of as an important measure to reduce post-operative complications and mortality, abdominal drainage was used widely after gastrectomy for gastric cancer in previous decades. The benefits of abdominal drainage have been questioned by researchers in recent years.OBJECTIVESThe objectives of this review were to access the benefits and harms of routine abdominal drainage post gastrectomy for gastric cancer.SEARCH STRATEGYWe searched the Cochrane Controlled Trials Register (Central/CCTR) in The Cochrane Library (2010, Issue 10), including the Specialised Registers of the Cochrane Upper Gastrointestinal and Pancreatic Diseases (UGPD) Group; MEDLINE (via Pubmed, 1950 to October, 2010); EMBASE (1980 to October, 2010); and the Chinese National Knowledge Infrastructure (CNKI) Database (1979 to October, 2010).SELECTION CRITERIAWe included randomised controlled trials (RCTs) comparing abdominal drain versus no drain in patients who had undergone gastrectomy (not considering the scale of gastrectomy and the extent of lymphadenectomy; irrespective of language, publication status, and the type of drain). We excluded RCTs comparing one drain with another.DATA COLLECTION AND ANALYSISFrom each trial, we extracted the data on the methodological quality and characteristics of the included studies, mortality (30-day mortality), re-operations, post-operative complications (pneumonia, wound infection, intra-abdominal abscess, anastomotic leak, drain-related complications), operation time, length of post-operative hospital stay and initiation of soft diet. For dichotomous data, we calculated the risk ratio (RR) and 95% confidence intervals (CI). For continuous data, we calculated mean differences (MD) and 95% CI. We tested heterogeneity using the Chi(2) test. We used a fixed-effect model for data analysis with RevMan software but we used a random-effects model if the P value of the Chi(2) test was less than 0.1.MAIN RESULTSWe included four RCTs involving 438 patients (220 patients in the drain group and 218 in the no-drain group).There was no evidence of a difference between the two groups in mortality (RR 1.73, 95% CI 0.38 to 7.84); re-operations (RR 2.49, 95% CI 0.71 to 8.74); post-operative complications (pneumonia: RR 1.18, 95% CI 0.55 to 2.54; wound infection: RR 1.23, 95% CI 0.47 to 3.23; intra-abdominal abscess: RR 1.27, 95% CI 0.29 to 5.51; anastomotic leak: RR 0.93, 95% CI 0.06 to 14.47); and initiation of soft diet (MD 0.15 day, 95% CI -0.07 to 0.37). However, the addition of a drain prolonged the operation time (MD 9.07 min, 95% CI 2.56 to 15.57) and post-operative hospital stay (MD 0.69 day, 95% CI 0.18 to 1.21) and lead to drain-related complications. Additionally, we should note that 30-day mortality and re-operations are very rare events and, as a result, very large numbers of patients would be required to make any sensible conclusions about whether the two groups were similar. The overall quality of the evidence according to the GRADE approach was "Very Low" for mortality and re-operations, and "Low" for post-operative complications, operation time, and post-operative length of stay.AUTHORS' CONCLUSIONSWe found no convincing evidence to support routine drain use after gastrectomy for gastric cancer.

Breast cancer is a heterogeneous disease with molecular subtypes that have biological distinctness and different behavior. The objective of this study is to evaluate the value of molecular subtypes in breast cancer management according to a retrospective analysis of breast carcinoma molecular subtypes, histopathological grade, and TNM stage. A retrospective study of 475 paraffin-embedded tissues of breast cancer samples from the First Affiliated Hospital of Guangxi Medical University was performed. Expression of ER, PR, Her-2 and Ki-67 was analyzed to classify molecular subtypes of breast cancer by immunohistochemistry. The differences of molecular subtypes of breast cancers in regard to TNM staging and pathological grade were analyzed using χ(2) tests. Values of P<0.05 were considered statistically significant. The frequency of luminal A, luminal B, HER2-positive luminal B, triple negative and non-luminal HER2-positive subtypes were: 35.5%, 22.5%, 13.1%, 15.2% and 13.7%, respectively. Among the five subtypes of breast cancer, the distribution of pathological grades showed a significant difference (P<0.001). There were significant differences in the distribution of TNM staging among the five subtypes of breast cancer (P<0.001). In addition to traditional prognostic indicators such as TNM staging and pathological grade, molecular subtype may aid clinical practice and research into breast cancer. Different molecular subtypes will lead to different prognosis and therapeutic option. Molecular subtyping is essential for breast cancer management.

Approximately 15% of gastrointestinal stromal tumors (GIST) do not express KIT mutations and of these about 5 to 7% harbor mutations in PDGFRA. DOG1 was specifically expressed in GISTs. These cases require special attention for PDGFRA and DOG1 mutational status. Hundred cases of GIST were diagnosed between August 2007 and October 2012 at the First Affiliated Hospital of Guangxi Medical University. DNA from tumor tissues and normal adjacent tissues was isolated and amplified for the 22 exons of PDGFRA and 26 exons of DOG1. Each PCR product was sequenced. Amino acid sequences were inferred from DNA and aligned to GenBank reference sequences to determine the position and type of mutations. Overall, 16.0% of the samples had a mutation in PDGFRA, and GISTs with mutations in the DOG1 gene were not found. Of the mutations detected, they were in PDGFRA exon 18 (8 cases, 8%), PDGFRA exon 12 (5 cases, 5%), PDGFRA exon 14 (1 cases, 1.0%), PDGFRA exon 11 (1 cases, 1.0%), and PDGFRA exon 8 (1 cases, 1.0%). Of these, Y392S, L521P and T632K mutant occurred in PDGFRA exon 8, exon 11 and exon 14, respectively. The mutation of PDGFRA has been considered as another causative genetic event as PDGFRA mutations were found in most GISTs lacking a KIT mutation. PDGFRA mutations occurred preferentially in exon 18 and exon 12. Mutations occurring in PDGFRA exon 8 (Y392S), exon 11 (L521P) and exon 14 (T632K) also were first identified. The over-expression of DOG1 was not related to DOG1 gene mutation.

Gastrointestinal stromal tumors (GISTs) are the most common primary mesenchymal tumors of the digestive tract. GISTs include a group of heterogeneous tumors with different morphology, biologic behavior, and genetic characteristics, so their epidemiology, clinico-pathological features and prognosis is distinct in different countries. The objective of this study is to analyze clinico-pathological characteristics and prognostic factors of GISTs among Chinese population. We investigated 112 GIST patients were diagnosed between July 2008 and January 2013 at the First Affiliated Hospital of Guangxi Medical University. Histologic evaluation and immunohistochemistry analysis was performed on paraffin-embedded tissue from the 112 GISTs. Overall survival analysis was carried out using the Kaplan-Meier method and the log-rank test. Multivariate analysis was performed according to Cox's proportional hazards model. Three and 5-year OS rates were 71.4 and 58.6% respectively. Univariate analysis showed that the following factors were significant in predicting OS: tumor site, tumor size, metastasis, resection margin status, cell type, invasion of adjacent organ, invasion of smooth muscle, mitotic rate, P53 and adjuvant therapy with imatinib (P<0.05). Multivariate analysis showed that tumor size, metastasis, resection margin status, mitotic rate, P53 and adjuvant therapy with imatinib were independent prognostic factors associated with OS. This may aid in the prediction of clinical evolution and guide treatments in patients with GIST in China.

目的 探讨肝血管瘤患者的流行病学及临床特点.方法 对广西医科大学第一附属医院东院及西院2003～2011年9年期间收治的肝血管瘤患者的临床资料进行回顾性调查,分析其流行病学及临床特点.结果 共818例肝血管瘤患者纳入分析,其中男398例(48.7％),女420例(51.3％).各年男女患者构成比差异无统计学意义(x2=9.912,P=0.271),但不同年龄组的性别分布差异有统计学意义(x2=18.791,P=0.000 1),大于60岁年龄组中男性多于女性.肝血管瘤无特殊临床表现,本组病例中有75例(9.2％)患者合并有自身免疫性疾病.本组患者的肝血管瘤直径为0.5～39.0 cm,中位直径为3.0 cm,肿瘤大小与患者性别有关(P＜0.05),女性大于男性患者.肿瘤发生部位以肝右叶最常见,占57.2％,肿瘤发生部位在不同性别的分布差异无统计学意义(P＞0.05).肝血管瘤以单发病灶最常见(70.0％),单发病灶中右叶病灶多于左叶病灶,多发病灶以双叶多发最常见.结论 肝血管瘤在性别、年龄、肿瘤大小、位置等方面具有一定的分布规律,应深入开展防治策略研究;对参与肝血管瘤发生、发展的相关因素有待深入研究;自身免疫性疾病与肝血管瘤的关系值得进一步探讨.

Objective To explore the prognostic factors of patients with primary retroperitoneal tumor(PRT) treated by surgical resection. Methods We retrospectively analyzed 80 patients with PRT treated in the First Affiliated Hospital of Guangxi Medical University between June 2001 and June 2012.Survival and prognosis were analyzed using the Kaplan-Meier method,the Cox proportional hazard model and the log-rank test. Results All patients were followed up for a median of 40.4 months, and the 1-, 3-, and 5-year cumulative survival rates were 92.5%,73.1% and 67.5%.Median survival time was 67 months. Univariate analysis identified the following significant predictors of survival(P<0.05): surgical method,tumor size,tumor characteristics,mitotic counts of tumor cells,and invasion of adjacent organs.Multivariate analysis identified the following independent prognostic factors(P<0.05):surgical method,tumor characteristics,mitotic counts of the tumor cells and invasion of adjacent organs. Conclusion Surgical resection is the most effective treatment for PRT.Tumor characteristics, surgical method,invasion of adjacent organs and mitotic counts of tumor cells are the most important prognostic factors for PRT.

Objective:To explore the association between aflatoxin B1(AFB1) exposure and the development of hepatocelluar carcinoma(HCC).Methods:Immunohistochemistry method was used to detect the levels of AFB1-DNA adducts.A total of 260 cases of HCC and non-HCC liver tissues were categorized into 4 groups according to their residency,HCC group(n=79) and controls(n=58) from Nanning area,HCC group(n=86) and controls(n=37) from Guilin area.Results:The AFB1-DNA adduct levels from Nanning area was significantly higher than those from Guilin area(χ2=31.042,P<0.001).The AFB1-DNA adduct levels of HCC and control groups from Nanning area were different(χ2=21.484,P<0.001),but there was no difference in AFB1-DNA adduct levels between HCC and control groups from Guilin area(χ2=0.318,P=0.573).Conclusion:There is a regional difference in AFB1 exposure in Guangxi,the AFB1-DNA adduct levels from Nanning area are much higher than those from Guangxi area.The AFB1 exposure is a risk factor for the hepatocarcinigenesis of HCC in Nanning area.

目的:探讨原发性肝细胞癌病理分化的临床影响因素。方法:采用病例回顾分析方法对317例原发性肝细胞癌患者进行临床资料调查;通过多分类有序Logistic回归模型进行单因素与多因素的分析。结果:单因素分析显示,15个因素中,年龄、体重、吸烟、饮酒、术前AFP水平及肝硬化与肝癌细胞分化有关;多因素分析显示,只有肝硬化存在相关性(P<0.05),无肝硬化及轻度肝硬化患者与中重度肝硬化患者的病理分化相比,其OR值分别是3.13和3.40。结论:肝硬化是肝癌细胞分化的一个影响因素。

目的:探讨肝组织石蜡切片8-OHdG免疫组织化学(免疫组化)染色的实验方法.方法:以皮肤组织作为阳性对照,PBS代替一抗作为阴性对照,采用4种不同实验条件在肝组织石蜡切片中行8-OHdG免疫组化方法染色.结果:实验条件3,即高温高压柠檬酸盐(pH6.0)缓冲液+胃蛋白酶K(10mg/L)的联合修复方法,并采用1%Triton X-100打孔过夜的方法能在肝组织中做出可靠阳性结果.结论:实验条件3为8-OHdG免疫组化染色取得可靠阳性结果的最合理的方法.