Hepatic resection for hepatocellular carcinoma exceeding Milan criteria

Delis, Spiros; Bakoyiannis, Andreas; Tassopoulos, Nikos; Athanassiou, Kostas; Kelekis, Dimitrios; Madariaga, Juan; Dervenis, Christos

doi:10.1016/j.suronc.2009.05.003

Cited by 29 publications

(26 citation statements)

References 38 publications

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“…5 Regarding HCCs > 50 mm in the present study, TACE + 3D-HDCRT led to 64% CR, 79% and 42% overall survival rates at one and 3-years (median, 30 months). Some published series reported that surgical resection of HCCs > 50 mm gives 69% and 37% overall survival rates at respectively 1 and 3-years (median, 20 months) 37,38 , thus at least comparable, although with a trends to inferiority, to our TACE + 3D-HDCRT data.…”

Section: Discussionsupporting

confidence: 82%

Efficacy and safety of transarterial chemoembolization combined to conformal radiotherapy for uninodular hepatocellular carcinoma

Merle

Rode

Benlaredj

et al. 2014

Int J Cancer Ther Oncol

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Original ArticleAbstract Purpose: A proportion of patients with uninodular hepatocellular carcinoma (HCC) cannot benefit from potential curative therapies such as liver transplantation, surgical resection or radiofrequency ablation. Thus, they are prone to receive transarterial chemoembolization (TACE) that is a palliative option with low probability of both complete response and prolonged local control. Herein, we assessed the combination of TACE and 3D-high dose conformal radiotherapy (3D-HDCRT) for efficacy and safety in HCC. Methods: We retrospectively analyzed the outcome of 35 consecutive patients with uninodular HCC ≤ 100 mm, treated by one course of TACE combined to 3D-HDCRT. The follow-up consisted on clinics, biology, hepatic CT-scan or MRI at month-1 and -3, and thereafter every 3 months. Results: Complete response was obtained in 80% of patients following mRE-CIST criteria (95% in HCC ≤ 50 mm, and 60% in HCC > 50 mm) with uncommon local recurrence (11%), overall survival rates of 79%, 59% and 44% at respectively 1, 2 and 3 years (median, 37.3 months), and 11.4% grade-3/4 toxicities. Pre-therapeutic α-fetoprotein level ≥ 200 ng/mL was found as a strong predictor of poorer outcome. Conclusion: We showed that TACE combined to 3D-HDCRT can be highly efficient to reach local control and interesting overall survival rates for uninodular HCC, with limited severe toxicities for Child-Pugh A patients. Subsequent prospective controlled trials are warranted for comparison with therapeutic standards.

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Section: Discussionsupporting

confidence: 82%

Efficacy and safety of transarterial chemoembolization combined to conformal radiotherapy for uninodular hepatocellular carcinoma

Merle

Rode

Benlaredj

et al. 2014

Int J Cancer Ther Oncol

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“…Due to an insidious onset, the majority of HCC patients are diagnosed at an advanced stage, which results in a <20% clinically resectable rate (11,12). With the exception of α-fetoprotein (AFP), at present, there remains a lack of well-recognized effective tumor markers for routine clinical detection of HCC.…”

Section: Discussionmentioning

confidence: 99%

Detecting abnormal methylation of tumor suppressor genes GSTP1, P16, RIZ1, and RASSF1A in hepatocellular carcinoma and its clinical significance

Jiang

et al. 2015

Oncology Letters

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Abstract. Hepatocellular carcinoma (HCC) has a high rate of mortality. Further studies into epigenetic changes in HCC, particularly the abnormal methylation of tumor suppressor genes (TSGs), are required, since these changes may provide novel biomarkers for early screening and diagnosis of HCC. By using methylation-specific polymerase chain reaction (MSP), the present study detected the methylation status in the promoter region of 4 candidate TSGs, GSTP1, P16, RIZ1, and RASSF1A, respectively, in 35 paired HCC and tumor-adjacent liver tissues in addition to 20 normal liver tissues. Their effect on the initiation and progression of HCC was also investigated by analyzing the clinicopathological data. The results of the present study revealed that the methylation level of RIZ1 and GSTP1 genes in HCC was significantly increased compared with that in the adjacent tissues (P<0.01) and the normal liver tissues (P<0.01). The methylation frequency of P16 and RASSF1A genes was not significantly increased compared with that observed in the adjacent tissues (P>0.05) but was significantly increased compared with the normal tissues (P<0.01). In HCC tissues, the methylation frequency of the GSTP1 gene in tumors with capsular invasion was significantly increased compared with that in tumors without capsular invasion (P<0.05). The methylation frequency of P16 gene in hepatitis B surface antigen (HbsAg)-positive HCC patients was significantly increased compared with that in HbsAg-negative patients (P<0.05). The methylation status of RIZ1 and RASSF1A genes was not significantly correlated with the clinicopathological data (P>0.05). Previous studies have demonstrated that the methylation status of RIZ1 and GSTP1 genes is HCC-specific, and thus may be used as a biomarker to assist the clinical diagnosis of HCC. While the methylation of GSTP1 gene promoter may associate with the invasiveness of HCC, chronic hepatitis B virus infection may be the cause of methylation-induced P16 inactivation. IntroductionHCC is one of the tumors with the highest incidence worldwide, and its incidence and mortality in China have remained high. The occurrence of HCC is results from multiple factors, including the activation of certain oncogenes, inactivation of TSGs and exogenous stimuli. Previous studies have demonstrated that the hypermethylation of CpG islands in tumor suppressor gene (TSG) promoters is closely associated with the formation of HCC, which may transform the spatial structure of chromatin and hence block/silence the transcription of TSGs via recruiting proteins of the methyl CpG binding domain (MBD) family in addition to the associated protein complexes (1,2). Epigenetic silencing is a relatively common mechanism of TSG inactivation (3). The aberrant methylation of tumor-associated genes, particularly TSGs, requires further research.A high frequency of methylation inactivation of the GSTP1 gene has been observed in human prostate, kidney, and liver cancers (4-6). Zhang et al (7) and Tchou et al (8) demonstrated that there is a high freq...

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“…Liver resection is still considered as the prime choice and the most effective “curative” treatment for HCC, especially for solitary large HCC [2]. Despite the improvement in treatment of HCC during recent decades, the overall survival of patients with HCC remains unsatisfactory due to high rate of recurrence and metastasis after liver resection [2, 3]. Thus, it is essential to explore effective biomarkers for recurrence and metastasis to improve treatment strategy for better clinical outcome.…”

Section: Introductionmentioning

confidence: 99%

JARID2 promotes invasion and metastasis of hepatocellular carcinoma by facilitating epithelial-mesenchymal transition through PTEN/AKT signaling

Xiong

Chang

et al. 2016

Oncotarget

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JARID2 is crucial for maintenance of pluripotency and differentiation of embryonic stem cells. However, little is known about the role of JARID2 in metastasis of hepatocellular carcinoma (HCC). This study found that JARID2 expression was significantly higher in HCC tissues than that in adjacent non-tumor liver tissues (ANLTs), and its expression level correlated with HCC metastasis. High JARID2 expression was significantly correlated with multiple tumor nodules, high Edmondson-Steiner grade, microvascular invasion, advanced TNM stage and advanced BCLC stage (all P < 0.05) and indicated poor prognosis of HCC in training and validation cohorts (all P < 0.05) totaling 182 patients. High JARID2 expression was an independent and significant risk factor for disease-free survival (DFS; P = 0.017) and overall survival (OS; P = 0.041) after curative liver resection in training cohort, and also validated as an independent and significant risk factor for DFS (P = 0.033) and OS (P = 0.031) in validation cohort. Moreover, down-regulation of JARID2 dramatically inhibited HCC cell migration, invasion, proliferation in vitro and metastasis in vivo, whereas overexpression of JARID2 significantly increased migration, invasion, proliferation in vitro and metastasis in vivo. Mechanistically, the data showed that JARID2 exerted its function by repressing PTEN expression through increasing H3K27 trimethylation (H3K27me3) at PTEN promoter region, which subsequently resulted in activation of protein kinase B (AKT) and enhanced epithelial-mesenchymal transition (EMT). In conclusion, this study revealed that JARID2 promotes invasion and metastasis of HCC by facilitating EMT through PTEN/AKT signaling.

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Hepatic resection for hepatocellular carcinoma exceeding Milan criteria

Cited by 29 publications

References 38 publications

Efficacy and safety of transarterial chemoembolization combined to conformal radiotherapy for uninodular hepatocellular carcinoma

Efficacy and safety of transarterial chemoembolization combined to conformal radiotherapy for uninodular hepatocellular carcinoma

Detecting abnormal methylation of tumor suppressor genes GSTP1, P16, RIZ1, and RASSF1A in hepatocellular carcinoma and its clinical significance

JARID2 promotes invasion and metastasis of hepatocellular carcinoma by facilitating epithelial-mesenchymal transition through PTEN/AKT signaling

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