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    [Genetic constitution analysis of idiopathic sudden hearing loss].
    (2010) Bora, Adem; Altuntaş, Emine Elif; Ozdemir, Oztürk; Uysal, Ismail Onder; Müderris, Suphi
    The purpose of this research is to understand the etiology of sudden hearing loss due to genetic factors in Turkish people. Determination of these genetic factors and better understanding of molecular pathogenesis may guide more realistic planning and treatment recommendations. Forty patients (Group 1; 19 males, 21 females; mean age 37.9+/-15.6 years; range 9 to 76 years) who presented with sudden hearing loss to the Ear, Nose and Throat Clinic of Medical Faculty Hospital of Cumhuriyet University between January 2008 and June 2009, and were diagnosed with sudden hearing loss through history, physical examination and review of audiometric findings, and 20 healthy volunteers (Group 2; 14 males, 6 females; mean age 31.7+/-4.4 years; range 24 to 43 years) for the control group were included in this study. All Patients were evaluated by the genetic clinic for the GJB2, GJB3, GJB6 and WFS1 gene using multiplex ligation-dependent probe amplification (MLPA) method mutation analysis. No difference was found in the peripheral blood sample analyses of the two groups at WFS1 exon 8 and connexin 26, 30 and 31 gene zones using the MLPA method with respect to heterozygous mutation (p=0.291, p>0.05). In four patients in group 1 heterozygous mutation was detected at the target gene zone. Heterozygous mutation was in the WFS1 exon 8 zone in two patients; and in the WFS1 exon 1 zone in other two patients. Sudden hearing loss studies in the future should include connexin 26, connexin 30 and other gene mutations that may affect the function of the gap-junction located in the region of the cochlea stria vascularis (stV), basal membrane (BM), spiral limbus (Li) and spiral ligament (SL). These studies should be performed on larger series, and should include family members of patients with sudden hearing loss.
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    Predictive significance of KRAS point mutation in patients with nonsmall cell lung carcinoma relation to smoking and asbestos exposure in middle anatolia population
    (2010) Arslan, Sulhattin; Akkurt, Ibrahim; Koksal, Binnur; Karadayi, Sule; Ozdemir, Oztürk
    Persons who have been occupationally exposed to environmental mutagens have a substantially increased risk for somatic oncogene mutations. Structural mutation in viral kristen rat sarcoma oncogene homolog 2 (KRAS; v-Ki-ras 2) has been assessed as a mechanism of de-novo resistance to epidermal growth factor receptor (EGFR) tyrosine-kinase inhibition in patients with non-smallcell lung cancer (NSCLC). The aim of the current study was to investigate the predictive significance of KRAS mutations in patient with NSCLC in relation to cigarette smoking and asbestos exposure. We have investigated 42 fresh tumoral tissue samples of cases that were histopathologically diagnosed as lung carcinomas. Patients were evaluated for clinical findings; tumoral tissue samples were examined histopathologically and genomic DNA from tumoral tissue samples were isolated. The KRAS point mutations were assessed by stripAssay reverse hybridization method and compared with the healthy controls. A total of 24 patients (57%) demonstrated KRAS point mutations in their tumoral tissues, while 18 (43%) patients did not. Mutations were accumulated in current cases of NSCLC, which were active smokers and exposed to the asbestos. Current results showed that the combined effects of somatic mutations in KRAS may play an active role in development of primary lung carcinomas due to heavy smoke and asbestos exposure. Results also may have important implications for molecular diagnosis and targeted therapies in NSCLC.