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

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.contributor.authorYavuzer, Dilek
dc.contributor.authorDemir, Gokhan
dc.contributor.authorDogusoy, Gulen
dc.contributor.authorArtac, Mehmet
dc.date.accessioned2023-02-21T12:39:59Z
dc.date.available2023-02-21T12:39:59Z
dc.date.issued2015-01-01
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
dc.description.abstract35G>C
dc.description.abstract35G>T
dc.description.abstract34G>A
dc.description.abstract34G>C
dc.description.abstract34G>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.
dc.description.issue6
dc.description.issueNOV
dc.description.pages1275-1279
dc.description.volume3
dc.identifier.doi10.3892/mco.2015.633
dc.identifier.urihttps://hdl.handle.net/11443/2565
dc.identifier.urihttp://dx.doi.org/10.3892/mco.2015.633
dc.identifier.wosWOS:000453159000014
dc.publisherSPANDIDOS PUBL LTD
dc.relation.ispartofMOLECULAR AND CLINICAL ONCOLOGY
dc.subjecthepatocellular carcinoma
dc.subjectK-Ras expression
dc.subjectmutation analysis
dc.subjectcetuximab
dc.titlePrevalence of K-Ras mutations in hepatocellular carcinoma: A Turkish Oncology Group pilot study
dc.typeArticle

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