Establishment and Validation of a Ferroptosis-Related lncRNA Signature for Prognosis Prediction in Lower-Grade Glioma.

Background: The prognosis of lower-grade glioma (LGG) is highly variable, and more accurate predictors are still needed. The aim of our study was to explore the prognostic value of ferroptosis-related long non-coding RNAs (lncRNAs) in LGG and to develop a novel risk signature for predicting survival with LGG. Methods: We first integrated multiple datasets to screen for prognostic ferroptosis-related lncRNAs in LGG. A least absolute shrinkage and selection operator (LASSO) analysis was then utilized to develop a risk signature for prognostic prediction. Based on the results of multivariate Cox analysis, a prognostic nomogram model for LGG was constructed. Finally, functional enrichment analysis, single-sample gene set enrichment analysis (ssGSEA), immunity, and m6A correlation analyses were conducted to explore the possible mechanisms by which these ferroptosis-related lncRNAs affect survival with LGG. Results: A total of 11 ferroptosis-related lncRNAs related to the prognosis of LGG were identified. Based on prognostic lncRNAs, a risk signature consisting of 8 lncRNAs was constructed and demonstrated good predictive performance in both the training and validation cohorts. Correlation analysis suggested that the risk signature was closely linked to clinical features. The nomogram model we constructed by combining the risk signature and clinical parameters proved to be more accurate in predicting the prognosis of LGG. In addition, there were differences in the levels of immune cell infiltration, immune-related functions, immune checkpoints, and m6A-related gene expression between the high- and low-risk groups. Conclusion: In summary, our ferroptosis-related lncRNA signature exhibits good performance in predicting the prognosis of LGG. This study may provide useful insight into the treatment of LGG.

In vivo and in vitro effects of microRNA-221 on hepatocellular carcinoma development and progression through the JAK-STAT3 signaling pathway by targeting SOCS3.

Hepatocellular carcinoma (HCC), as the third leading cancer-caused deaths, prevails with high mortality, and affects more than half a million individuals per year worldwide. A former study revealed that microRNA-221 (miR-221) was involved in cell proliferation of liver cancer and HCC development. The current study aims to evaluate whether miR-221 targeting SOCS3 affects HCC through JAK-STAT3 signaling pathway. A series of miR-221 mimic, miR-221 inhibitor, siRNA against SOCS3, and SOCS3 plasmids were introduced to SMMC7721 cells with the highest miR-221 expression assessed. The expression of JAK-STAT3 signaling pathway-related genes and proteins was determined by Western blot analysis. Cell apoptosis, viability, migration, and invasion were evaluated by means of flow cytometry, 3-(4,5-dimethylthiazol-2-yl)-2,5 diphenyl tetrazolium bromide, and transwell assays, respectively. HCC xenograft in nude mice was performed to measure HCC tumor growth. miR-221 was found to be highly expressed but SOCS3 was poorly expressed in HCC tissues. miR-221 expression was correlated with lymph node metastasis (LNM) and tumor node metastasis (TNM) of HCC, and SOCS3 expression was correlated with LNM, differentiation and TNM of HCC. SOCS3 is a target gene of miR-221. MiR-221 mimic or si-SOCS3 exposure was found to induce cell viability, migration, and invasion, and reduce apoptosis. MiR-221 inhibitor was observed to have inhibitory effects on HCC cell proliferation, migration, and invasion. Moreover, the expression of JAK-STAT3 signaling pathway was suppressed by miR-221 inhibitor. Downregulated miR-221 expression could promote its target gene SOCS3 to inhibit the proliferation, invasion and migration of HCC cells by repressing JAK-STAT3 signaling pathway.

Hepatic resection versus transarterial chemoembolization for patients with Barcelona Clinic Liver Cancer intermediate stage Child-Pugh A hepatocellular carcinoma.

The present study aimed to compare the overall and recurrence-free survival rates following hepatic resection (HR) and transcatheter arterial chemoembolization (TACE) in patients with Barcelona Clinic Liver Cancer (BCLC) classified intermediate-stage Child-Pugh A hepatocellular carcinoma (HCC). A total of 443 patients were examined, among whom 274 underwent HR, whereas 169 received TACE. The overall survival, recurrence-free survival between groups and subgroups, and risk factors with respect to mortality and recurrence, were analyzed. The 1-, 3- and 5-year overall and recurrence-free survival rates were 70, 46 and 37% and 73, 52, and 37%, respectively after HR, compared with 38, 15, and 12% and 44, 25 and 16%, respectively after TACE. Overall and recurrence-free survival rates were significantly increased following HR compared with TACE. Subgroup analysis in the multi-nodule group showed that the 1-, 3- and 5-year overall survival rates were 68, 38 and 30% after HR, compared with 36, 10 and 0% following TACE. In the solitary tumor group, 1-, 3- and 5-year overall survival rates were 71, 50 and 38% after HR, and 41, 22 and 15% after TACE. The overall survival rate after HR was significantly increased compared with that after TACE in the solitary tumor and multi-nodule groups. The risk factors for mortality include solitary tumor diameter >10 cm, multi-nodules, serum albumin level ≥35 g/l, prothrombin time >13 sec, alphafetoprotein levels >400 ng/ml, and patients with hepatitis B virus. Solitary tumor diameter >10 cm, multi-nodules, and hepatitis B virus (P<0.001) were found to be associated with higher recurrence of HCC. Overall and recurrence-free survival rates were improved after HR compared with those after TACE in BCLC stage B, Child-Pugh A, HCC patients.

miR-128-3p suppresses hepatocellular carcinoma proliferation by regulating PIK3R1 and is correlated with the prognosis of HCC patients.

microRNAs (miRNAs) are known to be involved in the pathogenesis of hepatocellular carcinoma (HCC). miR-128-3p was recently reported to be deregulated in several types of cancer. However, the biological function and potential mechanisms of miR-128-3p in HCC remain unknown. In the present study, we found that miR-128-3p was frequently downregulated in HCC tissues and cell lines by qRT-PCR analysis. Moreover, functional assays showed that overexpression of miR-128-3p markedly suppressed HCC cell proliferation by inducing G1 phase cell arrest and migration. Mechanistically, miR-128-3p was confirmed to regulate PIK3R1 (p85α) expression thereby suppressing phosphatidylinositol 3-kinase (PI3K)/AKT pathway activation using qRT-PCR and western blot analysis. Furthermore, correlation analysis and Kaplan-Meier estimates revealed an inverse correlation between miR-128-3p and p85α as well as a shorter disease-free survival (DFS) period after HCC resection in patients with low miR-128-3p expression. Hence, we conclude that miR-128-3p, which is frequently downregulated in HCC, inhibits HCC progression by regulating PIK3R1 and PI3K/AKT activation, and is a prognostic marker for HCC patients.

Primary hepatic non-Hodgkin's lymphoma with rectal cancer: A case report.

Primary hepatic non-Hodgkin's lymphoma (NHL) is an extremely rare disease that is commonly neglected as a possible diagnosis. The present study reports the case of a middle-aged male with chronic hepatitis B in which primary hepatic NHL and rectal cancer occurred simultaneously. A large solitary tumor in the left lobe of the liver was incidentally detected on routine examination prior to the laparoscopic resection of the rectal cancer. Laparoscopic resection of the rectal cancer and a liver biopsy were performed simultaneously. The pathology revealed that the hepatic tumor was NHL and that the rectal cancer was adenocarcinoma. Systemic staging revealed no evidence of nodal or bone marrow involvement, therefore, primary hepatic lymphoma (PHL) was diagnosed. PHL associated with rectal adenocarcinoma is extremely rare and to the best of our knowledge, has never been reported. At present, the cause and most effective therapy for the condition remain unclear.

Treatment efficacy and prognostic factors for huge HCC based on Barcelona Clinic Liver Cancer staging.

OBJECTIVE: To explore the most appropriate treatment for patients with hepatocellular cancer (HCC)>10 cm by using the Barcelona Clinic Liver Cancer (BCLC) classification. MATERIALS AND METHODS: A total of 124 HCC patients undergoing surgery were selected. Disease-free survival (DFS), overall survival (OS) and prognostic factors were respectively assessed. RESULTS: This study showed that the cumulative 1-, 3-, 5-year survival rates were 79.7%, 59.8% and 41.6% in BCLC-A patients, 76.2%, 9.5% and 0% in BCLC-B patients and 44.9%, 0% and 0% in BCLC-C patients, respectively. The 1-, 3-, 5-year DFS rates were 49%, 24.5% and 9.1% in BCLC-A patients, 7.5%, 0% and 0% in BCLC-B patients, respectively. No BCLC-C patients survived 1 year after surgery. Multivariate analysis indicated that hepatitis B surface antigen (HBsAg), vascular invasion, intra-hepatic metastasis, curative resection, tumor rupture and pathologic differentiation were independent prognostic factors. CONCLUSIONS: Surgery is effective and safe for patients with HCC>10 cm with sufficient hepatic reserve.

The glutathione S-transferase P1 341C>T polymorphism and cancer risk: a meta-analysis of 28 case-control studies.

BACKGROUND: GSTP1, which is one major group of the glutathione S-transferase family, plays an important role in the metabolism of carcinogens and toxins, reducing damage of DNA as a suppressor of carcinogenesis. The 341C>T polymorphism of the GSTP1 has been implicated in cancer risk through cutting down its metabolic detoxification activities. However, results from previous studies remain conflicting rather than conclusive. To clarify the correlation and provide more statistical evidence for detecting the significance of 341C>T, a meta-analysis was conducted. METHODOLOGY/PRINCIPAL FINDINGS: The relevant studies were identified through searching of PubMed, Embase, ISI Web of Knowledge and China National Knowledge Infrastructure in August 2012, and selected based on the established inclusion criteria for publications, then a meta-analysis was performed to quantitatively summarize the association of GSTP1 341C>T polymorphism with cancer susceptibility. Stratified analyses were employed to identify the source of heterogeneity. Publication bias was evaluated as well as sensitivity analysis. Based on 28 case-control studies with 13249 cases and 16798 controls, the pooled results indicated that the variant genotypes significantly increased the risk of cancer in homozygote comparison (TT versus CC: P = 0.012, OR = 1.40, 95% CI: 1.08-1.81, P(het.) = 0.575), and recessive model (TT versus CT/CC: P = 0.012, OR = 1.40, 95% CI: 1.08-1.81, P(het.) = 0.562). This was confirmed when stratified analyses were conducted according to ethnicity, source of control, matched control, quality score and cancer types. Moreover, significantly increased risk of cancer was also found in lung cancer (heterozygote comparison and dominant model). The stability of these observations was confirmed by a sensitivity analysis. Begger's funnel plot and Egger's test did not reveal any publication bias. CONCLUSIONS/SIGNIFICANCE: This meta-analysis suggests that the GSTP1 341C>T polymorphism may contribute to genetic susceptibility to cancer, especially to lung cancer, and in Asian population. Nevertheless, additional well-designed studies focusing on different ethnicity and cancer types are needed to provide a more exact and comprehensive conclusion.

Adjuvant imatinib for gastrointestinal stromal tumors: the current situation and problems.

OBJECTIVE: To review the current situation and find out the current problems of adjuvant imatinib for gastrointestinal stromal tumors (GISTs). METHODS: Searching for articles and records about imatinib for GISTs, especially adjuvant imatinib for GISTs, on MEDLINE, EMBASE and international conference on gastrointestinal. RESULTS: GISTs are derived from mesenchymal cells of the gastrointestinal tract. The standard treatment for primary GISTs is to resect the tumor together with the negative margins completely without tumor rupture and spillage. Conventional chemotherapy and radiotherapy is ineffective for advanced GISTs. The introduction of imatinib has dramatically changed the natural history of advanced GISTs. Imatinib is generally safe and effective with doses of 400, 600 or 800 mg daily, and has become the standard drug in the treatment for patients with advanced GISTs. Furthermore, most of the toxicity of imatinib is minimal and manageable, almost no treatment-related deaths have been reported. Therefore, adjuvant imatinib therapy is safe and seems to improve recurrence-free survival after the resection of primary GISTs. CONCLUSIONS: Although U.S Food and Drug Administration and European Medicines Agency have approved the use of adjuvant imatinib for GISTs postoperatively, a series of questions about the use of adjuvant imatinib still exist, such as the impact of adjuvant imatinib on overall survival, the optimal dose, the best duration of treatment and the most suitable patients. Doctors and patients should weigh the pros (the decrease of relapse) and cons (drug toxicity and drug costs), especially in terms of the benefit of overall survival.

Identifying serological biomarkers of hepatocellular carcinoma using surface-enhanced laser desorption/ionization-time-of-flight mass spectroscopy.

Lack of sensitive and specific biomarkers is a major reason for the high rate of hepatocellular carcinoma (HCC) related mortality. The aim of this study was to use surface-enhanced laser desorption/ionization-time-of-flight mass spectroscopy (SELDI-TOF-MS) technology to identify potential protein patterns specific for HCC. Eighty-one patients with hepatitis B-related HCC and 80 healthy controls were randomly divided into a training set (48 HCC, 47 controls) and a testing set (33 HCC, 33 controls). Serum proteomic profiles were measured using SELDI-TOF-MS. A classification tree was established by Biomarker Pattern Software. Candidate biomarkers were separated by HPLC and identified by MALDI-MS/MS and database searching. Forty-eight HCC cases, 54 liver cirrhosis cases and 42 healthy people were clinically validated using candidate biomarkers by SELDI-Immunoassay. Two up-regulated protein peaks were automatically chosen as a classification tree in the training set. These biomarkers were identified as thrombin light chain and growth related oncogene-alpha (GRO-alpha). The sensitivity and specificity of this classification tree were 89.6%. The multivariate model using the two biomarkers and AFP resulted in a sensitivity of 91.7% and specificity of 92.7%, which was significantly better than that of alpha-fetoprotein alone. We conclude that thrombin light chain and GRO-alpha are potential biomarkers of HCC.

[Evaluation of the risk of clonorchiasis inducing primary hepatocellular carcinoma].

OBJECTIVE: To explore the relationship between clonorchiasis and primary hepatocellular carcinoma (HCC) and analyze the synergistic actions of HBV infection, alcohol consumption and clonorchiasis on HCC development. METHODS: This hospital-based case-control study was conducted among 444 HCC patients (cases) and 500 non tumor patients (controls) to compare the prevalence of clonorchiasis in the cases and the controls. The risk of clonorchiasis and the synergistic actions between HBV infection, alcohol consumption and clonorchiasis on HCC development were analyzed by crossover analysis and multiple logistic regression. RESULTS: The prevalence of clonorchiasis in the cases (16.44%) was much higher than that of the controls (2.40%) (X2 = 56.58, P less than 0.01). In the case group, the OR value of those with clonorchiasis was 8.00 (95% CI: 4.34-14.92). The OR value was 4.82 (95% CI: 2.32-10.26) for the subjects whose clonorchiasis was diagnosed less than 10 years before their diagnosis of HCC, and was 17.54 (95% CI: 5.47-57.18) for those whose HCC was diagnosed more than 10 years ago. HBV infection, alcohol consumption and clonorchiasis showed an additive interaction in the development of HCC, with a relative excess risk of interaction of 110.43 and 18.23; attributable proportion of interaction of 0.80 and 0.63; synergy index of 5.18 and 2.84, respectively. CONCLUSION: Clonorchiasis could be an important risk factor for HCC. When the course of clonorchiasis is prolonged, the risk of HCC could increase. HBV infection, alcohol consumption and clonorchiasis might have synergistic actions on the development of HCC.

[Expression and significance of epidermal growth factor receptor variant type III in hepatocellular carcinoma].

BACKGROUND & OBJECTIVE: Many evidences show that epidermal growth factor receptor variant type III (EGFRvIII) plays an important role in initiation and progression of various cancers. But the relationship between EGFRvIII and hepatocellular carcinoma (HCC) is unclear. This study was to explore the expression and significance of EGFRvIII in human HCC tissues. METHODS: Immunohistochemical staining (IHC) was used to detect the expression of EGFRvIII in 55 specimens of HCC tissues and their adjacent non-cancerous liver tissues. RESULTS: Positive rate of EGFRvIII in HCC tissue was significantly higher than that in adjacent non-cancerous liver tissue [61.8% (34/55) vs. 38.2% (21/55), P < 0.05]. Positive rate of EGFRvIII in HCC tissue was significantly correlated with clinical stage,portal vein tumor thrombus,presence of extrahepatic metastasis, tumor recurrence, and the diameter of tumor, but not correlated with the number of foci, serum alpha-fetoprotein (AFP) level, serum HBsAg status, tumor differentiation, and cirrhosis in adjacent liver tissue. CONCLUSION: EGFRvIII is over-expressed in human HCC tissues, and relates to progression and recurrence of HCC.

[Expression and significance of EGF mRNA and EGFR mRNA in hepatocellular carcinoma].

BACKGROUND & OBJECTIVE: Many evidences demonstrated that the epidermal growth factor receptor (EGFR) subfamily played an important role in they initiation and progression of various cancers. But it is not clear whether there is a relationship between EGFR and hepatocellular carcinoma (HCC). The aims of the present study were to explore the expression and significance of the epidermal growth factor (EGF) mRNA and EGFR mRNA in human HCC tissues. METHODS: Reverse transcription polymerase chain reaction (RT-PCR) was employed to determine the expression of EGF mRNA and EGFR mRNA in 60 HCC tissues and their adjacent liver tissues. RESULTS: The positive rate of EGF mRNA was significantly lower in the HCC tissue (60%, 36/60) than in the adjacent liver tissue (80%, 48/60) (P< 0.05). The positive rate of EGFR mRNA in the HCC tissue (60%, 36/60) was markedly higher than in the adjacent liver tissue (41.67%, 25/60) (P< 0.05). The expression of EGFR mRNA in the HCC tissue was significantly correlated with the clinical stage, the portal vein tumor thrombus, the presence of extrahepatic metastasis, and the recurrence of tumor, the number of tumor, but not correlated with the diameter of tumor, the level of serum alpha-fetoprotein (AFP), the differentiation of tumor and the liver cirrhosis in the adjacent tissue. The detectable rate of EGF mRNA was correlated with the diameter of tumor but not correlated with the clinical stage, the portal vein tumor thrombus, the presence of extrahepatic metastasis, the recurrence of tumor, the number of tumor, the level of serum AFP, the differentiation of tumor and the liver cirrhosis in the adjacent tissue. CONCLUSIONS: EGF may not be involved in the initiation and progression of HCC, whereas, EGFR relates to the initiation and progression and the recurrence of HCC. EGFR can be considered as a marker for predicting the metastasis and recurrence of HCC.

[Comprehensive therapy for primary liver cancer: a report of 607 cases].

BACKGROUND & OBJECTIVE: Progress has been made in the field of early detection and early treatment of primary liver cancer (PLC), but many PLC patients remain unresectable, because their tumors are advanced or coexist with liver cirrhosis. Even if the tumor can be resected, the recurrent rate is more than 60%. This study aimed to investigate the efficacy of comprehensive therapy of PLC to improve the outcome. METHODS: A retrospective analysis of 607 patients with PLC received comprehensive treatment in Affiliated Tumor Hospital, Guangxi Medical University from 1985 to 2001. Among them, 423 cases were treated with various modes of hepatectomy: 134 with irregular hepatectomy, 95 with local radical resection, 123 with regular liver lobectomy or liver segment resection, 54 with semi-hepatectomy or more, 17 with hepatectomy combined with section of other organ. The other 184 nonresectable cases were treated with various combinations of therapy, such as ligation of hepatic artery, microwave coagulation, inter tumor injection of ethanol, cryosurgery, radio-frequency (RF), and intraperitoneal chemotherapy. RESULTS: 69.7%(423/607) of the whole group received liver resection, the overall mortality rate within one month after operation was 1.2%(5/423), and the 3-, 5-, 10-year survival rates were 42.7%(218/511), 37.5%(123/328), and 26.5%(26/98), respectively. For the resection group,the 3-, 5-, 10-year survival rates were 57.2%(203/355), 51.3%(118/230), and 35.3%(24/68), respectively. For the nonresectable group, the 3-, 5-, 10-year survival rates were 9.6%(15/156), 5.1%(5/98), and 6.7%(2/30), respectively. CONCLUSION: Surgery-predominant comprehensive therapy is effective modality for resectable PLC. Postoperative individualized comprehensive treatment can prevent tumor recurrence and improve postoperative effect.

[Study of anti-breast cancer activity of tumor infiltrating lymphocytes affected by dendritic cells].

BACKGROUND & OBJECTIVE: Dendritic cell (DC) is the strongest antigen presenting cell(APC). It can present antigen to T lymphocytes in vivo and in vitro,and induce cytotoxic T lymphocyte(CTL) reactions.This study was designed to investigate the killing activity of tumor infiltrating lymphocytes (TILs) stimulated by dendritic cells on breast cancer cells in vitro. METHODS: DCs were isolated from peripheral blood of patients with breast cancer. DCs were stimulated by granulocyte/macrophage colony stimulating factor (GM-CSF), interleukin-4(IL-4), and tumor antigen. Then TILs were stimulated by DCs and their killing activity on autogenous breast cancer cells and Bcap-37 breast cancer cells in vitro were observed. RESULTS: TILs stimulated by DCs had very high killing activity on autogenous breast cancer cells and the killing rate was (85.76+/-2.93)%. The killing rate was higher obviously than that of TILs not stimulated by DCs and T lymphocytes stimulated by DCs or not on autogenous breast cancer cells, respectively [killing rates: (52.11+/-1.48)%, (51.35+/-1.46)%, and (3.59+/-0.25)%, respectively]. However, their killing activities on Bcap-37 breast cancer cells were lower [killing rates: (40.03+/-1.29)%, (22.09+/-0.87)%, (21.66+/-0.85)%, and (1.76+/-0.14)%, respectively]. CONCLUSION: The results indicate that DC from the patients with breast cancer can induce TIL to produce efficient and specific anti-breast cancer immune response.

Genetic changes and expression of the mannose 6-phosphate/insulin-like growth factor II receptor gene in human hepatitis B virus-associated hepatocellular carcinoma.

It was reported that 60-70% of hepatitis B virus (HBV)-negative hepatocellular carcinoma (HCC) had loss of heterozygosity (LOH) at the mannose 6-phosphate/insulin-like growth factor II receptor (M6P/IGF2R) locus and this gene was mutated in 55% of these patients with LOH. In this study, genomic DNA from 29 pairs of HBV-positive HCC and corresponding non-tumor tissues was used to analyze LOH at the M6P/IGF2R locus and single deoxyguanosine deletion in this gene by PCR. Total RNA from 19 of the 29 patients was utilized to determine a 192 bp insert in the M6P/IGF2R mRNA and expression of this gene by RT-PCR. Twenty-eight of 29 (97%) HBV-positive HCC were found to be informative at the M6P/IGF2R locus but LOH at this region was only detected in 4/28 (14%) informative patients. Neither single deoxyguanosine deletion in this gene nor 192 bp insert in its mRNA occurred in these patients. Compared with corresponding non-tumor tissues, expression of the M6P/IGF2R mRNA was decreased in 13/19 (68%) HBV-positive HCC tissues, suggesting that M6P/IGF2R may be involved in HBV-associated hepatocarcinogenesis by the regulation of its expression level. In the development of HBV-associated HCC, M6P/IGF2R mutation may not be a major agent.

[Surgery-predominant comprehensive therapy for 134 patients with small hepatocellular carcinoma].

BACKGROUND & OBJECTIVE: Although surgical resection is the primary choice modality in treatment of small hepatocellular carcinoma(HCC), the 5-year recurrent rate after resection was as high as 35.4%-43.5%. This study was designed to investigate the efficacy of surgery-predominant comprehensive therapy for small HCC in reducing the recurrent rate and improving the outcome. METHODS: A total of 134 cases of small HCC (< or = 5 cm in diameter) received surgery-predominant comprehensive treatment in The Affiliated Tumor Hospital, Guangxi Medical University from 1985 to 2001. The median age of the patients was 45 years old (range,18-70 years). Of 134 cases, 121 were treated with hepatectomy: 16 with irregular hepatectomy, 83 with local radical resection, 12 with regular liver lobe resection or liver segment resection, 2 with left semi-hepatectomy, and 8 with hepatectomy and gallbladder resection. In the other 13 cases of nonresectable small HCC, they received multimodality treatments by various combinations of hepatic artery ligation and anticancer agents by hepatic artery infusion, microwave coagulation, ethanol injection into tumor, cryosurgery,radio-frequency (RF), and hepatic artery chemoembolization therapy. RESULTS: Of 134 HCC patients, 90.3% received liver resection and no operative death occurred. For the surgery group, the 1-, 3-, 5-, and 10-year survival rates were 89.3%, 74.4%, 64.6%, and 43.8%, respectively; the 1-, 3-, and 5-year recurrent rates were 11.9%, 23.8%, and 32.1%, respectively. For the total group,the 1-, 3-,5-, and 10-year survival rates were 88.8%, 72.2%, 63.4%, and 41.7%, respectively; the 1-, 3-, and 5-year recurrent rates were 15.9%, 29.1%, and 36.6%, respectively. CONCLUSIONS: Surgical resection remains primary choice modality in treatment of small HCC; postoperative comprehensive treatment is important for preventing tumor recurrence and improving the long-term results.