Prevalence of K-Ras mutations in hepatocellular carcinoma: A Turkish Oncology Group pilot study

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dc.contributor.authorTurhal, Nazi Serdar
dc.contributor.authorSavas, Berna
dc.contributor.authorCoskun, Oznur
dc.contributor.authorBas, Emine
dc.contributor.authorKarabulut, Bulent
dc.contributor.authorNart, Deniz
dc.contributor.authorKorkmaz, Taner
dc.date.accessioned2024-02-23T14:35:26Z
dc.date.available2024-02-23T14:35:26Z
dc.date.issued2015
dc.departmentNEÜen_US
dc.description.abstractHepatocellular carcinoma (HCC) is the fifth most common male-predominant type of cancer worldwide. There is no effective treatment regimen available for advanced-stage disease and chemotherapy is generally ineffective in these patients. The number of studies on the prevalence of K-Ras mutations in HCC patients is currently limited. A total of 58 patients from 6 comprehensive cancer centers in 4 metropolitan cities of Turkey were enrolled in this study. Each center committed to enroll approximately 10 random patients whose formalin-fixed paraffin-embedded tumor tissues were available for K-Ras, exon 2 genotyping. Two methods were applied based on the availability of adequate amounts of tumor DNA. In the first method, the samples were processed using TheraScreen. The genomic DNA was further used to detect the 7 most frequent somatic mutations (35G>A; 35G>C; 35G>T; 34G>A; 34G>C; 34G>T and 38G>A) in codons 12 and 13 in exon 2 of the K-Ras oncogene by quantitative polymerase chain reaction (PCR). In the second method, the genomic DNA was amplified by PCR using primers specific for K-Ras exon 2 with the GML SeqFinder Sequencing System's KRAS kit. The identified DNA sequence alterations were confirmed by sequencing both DNA strands in two independent experiments with forward and reverse primers. A total of 40 samples had adequate tumor tissue for the mutation analysis. A total of 33 (82.5%) of the investigated samples harbored no mutations in exon 2. All the mutations were identified via a direct sequencing technique, whereas none were identified by TheraScreen. In conclusion, in our patients, HCC exhibited a remarkably low (<20%) K-Ras mutation rate. Patients harboring K-Ras wild-type tumors may be good candidates for treatment with epidermal growth factor inhibitors, such as cetuximab.en_US
dc.identifier.doi10.3892/mco.2015.633
dc.identifier.endpage1279en_US
dc.identifier.issn2049-9450
dc.identifier.issn2049-9469
dc.identifier.issue6en_US
dc.identifier.pmid26807232en_US
dc.identifier.scopusqualityQ3en_US
dc.identifier.startpage1275en_US
dc.identifier.urihttps://doi.org/10.3892/mco.2015.633
dc.identifier.urihttps://hdl.handle.net/20.500.12452/16030
dc.identifier.volume3en_US
dc.identifier.wosWOS:000453159000014en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherSpandidos Publ Ltden_US
dc.relation.ispartofMolecular And Clinical Oncologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectHepatocellular Carcinomaen_US
dc.subjectK-Ras Expressionen_US
dc.subjectMutation Analysisen_US
dc.subjectCetuximaben_US
dc.titlePrevalence of K-Ras mutations in hepatocellular carcinoma: A Turkish Oncology Group pilot studyen_US
dc.typeArticleen_US

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