Özen, ÇiğdemYıldız, GökhanDağcan, Alper TungaÇevik, DilekÖrs, AyşegülKeleş, UmutTopel, HandeÖztürk, Mehmet2016-02-082016-02-0820131871-6784http://hdl.handle.net/11693/20956Conference Name: 15th European Congress on Biotechnology, (ECB15) 2012Date of Conference: 23-26 September 2012Hepatocellular carcinoma (HCC) represents a major form of primary liver cancer in adults. Chronic infections with hepatitis B (HBV) and C (HCV) viruses and alcohol abuse are the major factors leading to HCC. This deadly cancer affects more than 500,000 people worldwide and it is quite resistant to conventional chemo- and radiotherapy. Genetic and epigenetic studies on HCC may help to understand better its mechanisms and provide new tools for early diagnosis and therapy. Recent literature on whole genome analysis of HCC indicated a high number of mutated genes in addition to well-known genes such as TP53, CTNNB1, AXIN1 and CDKN2A, but their frequencies are much lower. Apart from CTNNB1 mutations, most of the other mutations appear to result in loss-of-function. Thus, HCC-associated mutations cannot be easily targeted for therapy. Epigenetic aberrations that appear to occur quite frequently may serve as new targets. Global DNA hypomethylation, promoter methylation, aberrant expression of non-coding RNAs and dysregulated expression of other epigenetic regulatory genes such as EZH2 are the best-known epigenetic abnormalities. Future research in this direction may help to identify novel biomarkers and therapeutic targets for HCC.EnglishChronic infectionDNA hypomethylationHepatocellular carcinomaPrimary liver cancersPromoter methylationRegulatory genesTherapeutic targetsWhole genome analysisAlkylationDiseasesNucleic acidsVirusesGene expressionAXIN1 proteinCyclin dependent kinase inhibitor 2AProtein p53Regulator proteinTranscription factor EZH2Unclassified drugUntranslated RNACancer geneticsChromosome aberrationDNA methylationEpigeneticsGain of function mutationGene expression regulationGene frequencyGenetic associationGenome analysisHepatitis B virusLiver carcinogenesisLiver cell carcinomaLoss of function mutationNonhumanPriority journalPromoter regionVirus DNA cell DNA interactionVirus genomeCarcinomaGenetic epigenesisGeneticsCarcinomaEpigenesisEpigenomicsHumanLiver neoplasmsArticle10.1016/j.nbt.2013.01.007