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| 1 | Significance of hepatitis virus infection in the oncogenicinitiation of hepatocellular carcinoma显示文摘Hepatocellular carcinoma(HCC) is one of the most common causes of cancer-related death worldwide. Chronic infection of hepatitis B virus(HBV) and/or hepatitis C virus(HCV) is a major risk factor in the development of the HCC, independently from excessive alcohol abuse and metabolic disease. Since the biology of HBV and HCV is different, their oncogenic effect may go through different mechanisms, direct and/or indirect. Viral hepatitis infection is associated with cellular inflammation, oxidative stress, DNA damage, that may lead to subsequent hepatic injuries such as chronic hepatitis, fibrosis, cirrhosis, and finally HCC. Direct oncogenic properties of these viruses are related with their genotypic characteristics and the ability of viral proteins to interact with host proteins, thus altering the molecular pathways balance of the cells. In addition, the integration of HBV DNA, especially the gene S and X, in a particular site of the host genome can disrupt chromosomal stability and may activate various oncogenic mechanisms, including those in hematopoietic cells. Recently, several studies also had demonstrated that viral hepatitis could trigger the population of hepatic cancer stem cells. This review summarize available pre-clinical and clinical data in literature regarding oncogenic properties of HBV and HCV in the early initiation of HCC. | Caecilia HC Sukowati Korri E El-Khobar Susan I Ie Beatrice Anfuso David H Muljono Claudio Tiribelli | 2016 | World Journal of Gastroenterology2016，22，4： | 18 |
| 2 | Hepatic cancer stem cells and drug resistance: Relevance in targeted therapies for hepatocellular carcinoma显示文摘Hepatocellular carcinoma (HCC) is one of most common malignancies in the world. Systemic treatments for HCC, particularly for advanced stages, are limited by the drug resistance phenomenon which ultimately leads to therapy failure. Recent studies have indicated an association between drug resistance and the existence of the cancer stem cells (CSCs) as tumor initiating cells. The CSCs are resistant to conventional chemotherapies and might be related to the mechanisms of the ATP Binding Cassette (ABC) transporters and alterations in the CSCs signaling pathways. Therefore, to contribute to the development of new HCC treatments, further information on the characterization of CSCs, the modulation of the ABC transporters expression and function and the signaling pathway involved in the self renewal, initiation and maintenance of the cancer are required. The combination of transporters modulators/inhibitors with molecular targeted therapies may be a potent strategy to block the tumoral progression. This review summarizes the association of CSCs, drug resistance, ABC transporters activities and changes in signaling pathways as a guide for future molecular therapy for HCC. | Caecilia HC Sukowati Natalia Rosso Lory S Crocè Claudio Tiribelli | 2010 | World Journal of Hepatology2010，2，3： | 16 |
| 3 | Computed Tomography Perfusion Imaging of Renal Cell Carcinoma: Systematic Comparison With Histopathological Angiogenic and Prognostic Markers显示文摘 | Caecilia S. Reiner Matthias Roessle Thore Thiesler Daniel Eberli Ernst Klotz Thomas Frauenfelder Tullio Sulser Holger Moch Hatem Alkadhi | 2013 | Investigative Radiology2013，，4： | 2 |
| 4 | Role of hepatitis B virus in development of hepatocellular carcinoma:Focus on covalently closed circular DNA显示文摘Chronic infection with hepatitis B virus(HBV)remains a major global health problem,especially in developing countries.It may lead to prolonged liver damage,fibrosis,cirrhosis,and hepatocellular carcinoma.Persistent chronic HBV infection is related to host immune response and the stability of the covalently closed circular DNA(cccDNA)in human hepatocytes.In addition to being essential for viral transcription and replication,cccDNA is also suspected to play a role in persistent HBV infections or hepatitis relapses since cccDNA is very stable in non-dividing human hepatocytes.Understanding the pathogenicity and oncogenicity of HBV components would be essential in the development of new diagnostic tools and treatment strategies.This review summarizes the role and molecular mechanisms of HBV cccDNA in hepatocyte transformation and hepatocarcinogenesis and current efforts to its detection and targeting. | Claryssa Bianca Elizabeth Sidhartha Claudio Tiribelli Korri Elvanita El-Khobar Caecilia H C Sukowati | 2022 | World Journal of Hepatology2022，14，5： | 1 |
| 5 | Clinical presentation and treatment outcome of sleeping sickness in Sudanese pre-school children显示文摘 | Gilles Eperon Caecilia Schmid Louis Loutan | 2007 | Acta Tropica2007，101，1： | 1 |
| 6 | The cardiac isoform of α-actin in regenerating and atrophic skeletal muscle, myopathies and rhabdomyomatous tumors: an immunohistochemical study using monoclonal antibodies显示文摘 | Roland Moll Hans-Jürgen Holzhausen Hans-Dieter Mennel Caecilia Kuhn Renate Baumann Christiane Taege Werner W. Franke | 2006 | Virchows Archiv2006，，2： | 1 |
| 7 | Exergy analysis of biomass-to-synthetic natural gas (SNG) process via indirect gasification of various biomass feedstock显示文摘 | Caecilia R Vitasari Martin Jurascik Krzysztof J Ptasinski | 2011 | Energy2011，36，6： | 1 |
| 8 | Hepatitis B virus genotypes in precision medicine of hepatitis Brelated hepatocellular carcinoma:Where we are now显示文摘Hepatitis B virus(HBV)infection is a major player in chronic hepatitis B that may lead to the development of hepatocellular carcinoma(HCC).HBV genetics are diverse where it is classified into at least 9 genotypes(A to I)and 1 putative genotype(J),each with specific geographical distribution and possible different clinical outcomes in the patient.This diversity may be associated with the precision medicine for HBV-related HCC and the success of therapeutical approaches against HCC,related to different pathogenicity of the virus and host response.This Editorial discusses recent updates on whether the classification of HBV genetic diversity is still valid in terms of viral oncogenicity to the HCC and its precision medicine,in addition to the recent advances in cellular and molecular biology technologies. | Caecilia H C Sukowati Sri Jayanti Turyadi Turyadi David H Muljono Claudio Tiribelli | 2024 | World Journal of Gastrointestinal Oncology2024，16，4： | 0 |
| 9 | Immunotherapy against programmed death-1/programmed death ligand 1 in hepatocellular carcinoma: Importance of molecular variations, cellular heterogeneity, and cancer stem cells显示文摘Hepatocellular carcinoma(HCC)is a heterogeneous malignancy related to diverse etiological factors.Different oncogenic mechanisms and genetic variations lead to multiple HCC molecular classifications.Recently,an immune-based strategy using immune checkpoint inhibitors(ICIs)was presented in HCC therapy,especially with ICIs against the programmed death-1(PD-1)and its ligand PD-L1.However,despite the success of anti-PD-1/PD-L1 in other cancers,a substantial proportion of HCC patients fail to respond.In this review,we gather current information on biomarkers of anti-PD-1/PD-L1 treatment and the contribution of HCC heterogeneity and hepatic cancer stem cells(CSCs).Genetic variations of PD-1 and PD-L1 are associated with chronic liver disease and progression to cancer.PD-L1 expression in tumoral tissues is differentially expressed in CSCs,particularly in those with a close association with the tumor microenvironment.This information will be beneficial for the selection of patients and the management of the ICIs against PD-1/PD-L1. | Caecilia H C Sukowati Korri Elvanita El-Khobar Claudio Tiribelli | 2021 | World Journal of Stem Cells2021，13，7： | 0 |
| 10 | MutL homolog 1 methylation and microsatellite instability in sporadic colorectal tumors among Filipinos显示文摘BACKGROUND Colorectal cancer(CRC)ranks third in terms of incidence and second in mortality worldwide.In CRC,the silencing of mismatch repair genes,including the mutL homolog 1(hMLH1)has been linked to microsatellite instability(MSI),the lengthening or shortening of microsatellite repeats.Very limited data have been presented so far on the link of hMLH1 methylation and MSI in Southeast Asia populations with sporadic CRC,and on its clinical significance.AIM To investigate the significance of the MSI status and hMLH1 methylation in CRC Filipino patients.METHODS Fifty-four sporadic CRC patients with complete clinical data were included in this study.Genomic DNA from CRC tumor biopsies and their normal tissue counterparts were profiled for MSI by high resolution melting(HRM)analysis using the Bethesda Panel of Markers(BAT25,BAT26,D2S123,D5S346,and D17S250).hMLH1 methylation screening was performed using bisulfite conversion and methylation specific polymerase chain reaction.Statistical analysis was conducted to calculate their associations to clinicopathological characteristics and survival relevance(Kaplan-Meier curves and the log-rank test).RESULTS hMLH1 methylation was observed in 9%and 35%of CRC and normal samples,respectively.Higher incidence of consistently methylated hMLH1 found in both normal and CRC was noticed for relation to location of tumor(P<0.05).As for MSI status,D2S123 the most common unstable microsatellite and MSI-high(MSIH)was the most common MSI profile,counted for 46%and 50%of normal and CRC tissues,respectively.The presence of MSI-low(MSI-L)and microsatellite stable(MSS)was 43%and 11%for normal,and 31%and 19%for CRC samples.The mean month of patients’survival was shorter in patients whose normal and tumor tissues had methylated compared to those with unmethylated hMLH1 and with MSI-H compared to those with MSI-L/MSS(P<0.05).This was supported by significant difference in Kaplan-Meier with log-rank analysis.This data indicated that hMLH1 methylation and high MSI status have prognostic value.CONCLUSION This study showed the clinical significance of hMLH1 methylation and MSI status in sporadic CRC Filipino patients,especially in the normal part of the tumor. | Loraine Kay D Cabral Cynthia A Mapua Filipinas F Natividad Caecilia H C Sukowati Edgardo R Cortez Ma Luisa D Enriquez | 2021 | World Journal of Gastrointestinal Oncology2021，13，12： | 0 |
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