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Permanent URI for this collectionhttps://hdl.handle.net/11443/932

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Author: search.filters.author.Yakicier, M. CengizHas files: No

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    PTPRD is Homozygously Deleted and Epigenetically Downregulated in Human Hepatocellular Carcinomas
    (MARY ANN LIEBERT, INC, 2015-01-01) Acun, Tolga; Demir, Kubilay; Oztas, Emin; Arango, Diego; Yakicier, M. Cengiz
    PTPRD (protein tyrosine phosphatase, receptor type, D) is a tumor suppressor gene, frequently inactivated through deletions or epigenetic mechanisms in several cancers with importance for global health. In this study, we provide new and functionally integrated evidence on genetic and epigenetic alterations of PTPRD gene in hepatocellular carcinomas (HCCs). Importantly, HCC is the sixth most common malignancy and the third most common cause of cancer-related mortality worldwide. We used a high throughput single nucleotide polymorphism (SNP) microarray assay (Affymetrix, 10K2.0 Assay) covering the whole genome to screen an extensive panel of HCC cell lines (N=14 in total) to detect DNA copy number changes. PTPRD expression was determined in human HCCs by Q-RT-PCR and immunohistochemistry. Promoter hypermethylation was assessed by combined bisulfite restriction analysis (COBRA). DNA methyl transferase inhibitor 5-azacytidine (5-AzaC) and/or histone deacetylase inhibitor Trichostain A (TSA) were used to restore the expression. We identified homozygous deletions in Mahlavu and SNU475 cells, in the 5 ` UTR and coding regions, respectively. PTPRD mRNA expression was downregulated in 78.5\% of cell lines and 82.6\% of primary HCCs. PTPRD protein expression was also found to be lost or reduced in HCC tumor tissues. We found promoter hypermethylation in 22.2\% of the paired HCC samples and restored PTPRD expression by 5-AzaC and/or TSA treatments. In conclusion, PTPRD is homozygously deleted and epigenetically downregulated in HCCs. We hypothesize PTPRD as a tumor suppressor candidate and potential cancer biomarker in human HCCs. This hypothesis is consistent with compelling evidences in other organ systems, as discussed in this article. Further functional assays in larger samples may ascertain the contribution of PTPRD to hepatocarcinogenesis in greater detail, not to forget its broader importance for diagnostic medicine and the emerging field of personalized medicine in oncology.
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    Serum Bone Markers Levels and Bone Mineral Density in Familial Mediterranean Fever
    (SOC PHYSICAL THERAPY SCIENCE, 2014-01-01) Aydin, Teoman; Taspinar, Ozgur; Akbal, Yildiz; Peru, Celaleddin; Guler, Mustafa; Uysal, Omer; Yakicier, M. Cengiz
    {[}Purpose] The aim of this study was to measure bone mineral density, serum and urinary bone turnover parameters, and to evaluate the influence of demographic and genetic factors on these parameters in FMF patients. {[}Subjects and Methods] Twenty-seven attack-free patients who were diagnosed with FMF (in accordance with Tel Hashomer criteria) were recruited at outpatient rheumatology clinics. We investigated whether there were any differences between the FMF patients and a control group in terms of lumbar and femur bone mineral density (BMD), standard deviation scores (Z scores and T scores) and bone markers. {[}Results] In terms of the median values of lumbar BMD (p = 0.21), lumbar T (p = 0.098) and Z (p = 0.109) scores, femoral neck BMD, femoral T and Z scores and total femur BMD, T (p = 0.788) and Z scores, there were no significant differences. {[}Conclusion] In our study, no statistically significant differences were found between FMF patients and a control group in terms of osteoporosis. The 25-OH vitamin D was found to be significantly lower in FMF patients than in the control group.