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Publications (5)4.71 Total impact

  • Zeynep Yegin, Sezgin Gunes, Recep Buyukalpelli
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    ABSTRACT: Bladder cancer like other cancers arises from the accumulation of many genetic and epigenetic changes that lead to the activation of proto-oncogenes or inactivation of tumor suppressor genes. We aimed to investigate the methylation patterns of Twist homolog 1 (TWIST1) and nidogen-2 (NID2) genes in bladder cancer. Fifty six histologically confirmed bladder tumor samples and paired 24 urine samples constituted the study group and was compared with 15 age- and gender-matched noncancerous individuals. DNA was purified from both tumor and urine samples. The methylation status of the two genes was analyzed by methylation-specific polymerase chain reaction (MSP) in both urinary bladder cell carcinoma samples and urine samples. Sensitivity and specificity values of the method were assessed and compared with the results of the cytology test. Methylation of TWIST1 and NID2 was detected in 98.2% and 96.4% of the tumor samples, and in 87.5% and 95.8% of the urine samples, respectively. The sensitivity of TWIST1 and NID2 genes (87.5% and 95.8% in urine samples, respectively), was higher compared with urine cytology (62.5%) for cancer detection. The sensitivity of any of the two genes was 88.8% (8/9) for low-grade cases. The sensitivity of urine cytology was 33.3% for the same low-grade cases. To be used in the early noninvasive diagnosis of bladder cancer, the combined methylation analysis of TWIST1 and NID2 genes may be a simple, noninvasive, sensitive, and specific method for detecting cancer cells in urine.
    DNA and cell biology 05/2013; · 2.28 Impact Factor
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    ABSTRACT: ErbB receptor tyrosine kinases family plays an important role in cell cycle regulation. Overexpression of ErbB receptors has been described in several solid tumors. The aim of this study was to investigate the levels of ErbB1, ErbB2, ErbB3, and ErbB4 expression in bladder cancer. Urinary bladder tumor samples were obtained from 33 bladder cancers and 7 non-cancerous bladder biopsies. The levels of ErbB1, ErbB2, ErbB3, and ErbB4 genes expression in bladder cancer were determined by real-time PCR. The presence of protein was confirmed by immunostaining. Expression of ErbB1, ErbB2, ErbB3, and ErbB4 genes increased 0.67, 4.72, 2.89, and 2.65-fold, respectively, in bladder tumors as compared with normal tissue. There was a significant difference between immunostaining results of ErbB4 protein in bladder tumors and normal bladder tissue (P<0.01). The present data suggest that ErbB2, ErbB3, and ErbB4 genes may have a role in bladder cancer tumorigenesis.
    Pathology - Research and Practice 01/2013; · 1.21 Impact Factor
  • Z. Yegin, S. Gunes, R. Buyukalpelli
    European Human Genetics Conference; 06/2012
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    ABSTRACT: High levels of SOX4 gene expression have been reported in a variety of human cancers. The protein may function in the apoptosis pathway, leading to cell death as well as to tumorigenesis. The aim of this study was to investigate the levels of SOX4 expression in bladder cancer. Urinary bladder tumor samples were obtained from 57 bladder cancer and 13 normal bladder biopsies. The levels of SOX4 expression in bladder cancer were determined by immunohistochemistry and real-time PCR. SOX4 gene expression was increased 2.2 times in bladder tumors as compared with normal tissue. The presence of protein was confirmed by immunostaining. There were significant differences between immunostaining of bladder tumors and normal bladder tissue (P=0.001). The present data suggest that SOX4 gene may have a role in bladder cancer tumorigenesis.
    Pathology - Research and Practice 06/2011; 207(7):423-7. · 1.21 Impact Factor
  • Gunes S, Buyukalpelli R, Yegin Z
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    ABSTRACT: Bladder cancer is the second most common malignancy of the urinary system and the fourth leading cause of cancer. Development and progression of bladder cancer is a multistage process and involves molecular (cell cycle regulatory proteins, such as CABLES, Ki67, and cyclin D1 gene) and genetic abnormalities (oncogenes such as TP63, FGFR3, EGFR, Ras, PIK3CA, MDM2; tumor suppressor genes, including TP53, RB1, CDKN2A/ARF, PTEN and FHIT), chemical and environmental exposures (aromatic amines, aniline dyes, nitrites, nitrates, acrolein, coal, arsenic, and cigarette smoking) or chronic irritation. In addition, it is shown that the microsatellite instability and multiple epigenetic factors may affect development and progression of bladder cancer. The purpose of this review is to highlight the most important molecular and genetic alterations in both low-grade noninvasive and high grade muscle-invasive tumors and molecular mechanisms that have been studied and reported recently, including a discussion of how these may define distinct genetic pathways of bladder cancer.
    01/2010: pages 119-136;