Sürdürülebilir Kalkınma Amaçları

• 2

Yazarlar

• Akkiprik, Mustafa(2)
• Karabulut, Sevgi(2)
• Kaya, Handan(2)
• Kaya, Zehra(2)
• Peker, Irem(2)
• Alış, Halil(1)
• Amuran, Gökçe Gullu(1)
• Büyükaşık, Süleyman(1)
• Dirican, Ebubekir(1)
• Erzik, Can(1)
• Gullu Amuran, Gokce(1)
• Gulluoglu, Bahadır M.(1)
• Gulluolu, Bahadir M.(1)
• Kankaya, Burak(1)
• Ozer, Ayse(1)
• Ozer, Ayşe(1)
• Ozmen, Tolga(1)
• Velidedeoğlu, Mehmet(1)
• Özmen, Tolga(1)
• İlvan, Ahmet(1)
• İlvan, Sennur(1)

• MakaleAçık Erişim2020Scopus SJRQ4/r/bayburt/13326
  Investigation of alterations in PIK3CA and OCT-4 gene expression in breast cancer

  Dirican, Ebubekir; Kankaya, Burak; Büyükaşık, Süleyman; Alış, Halil; Velidedeoğlu, Mehmet; İlvan, Sennur; İlvan, Ahmet

  Breast cancer (BCa) is one of the most prevalent cancer amongst women and PIK3CA mutations have a crucial role in carcinogenesis. On the other hand, Octamer-Binding Transcription Factor 4 (OCT-4) is common biomarkers of cancer stem cells, which provide to the pathological processes of numerous carcinomas. In this study, we evaluated the association of OCT-4 gene expression levels with the PIK3CA mutation in BCa patients. The mRNA expression level of the OCT-4 gene was detected by qPCR in 44 BCa patients and 30 BCa patients control have positive PIK3CA mutations. Exon 9 and exon 20 of PIK3CA mutations were identified by sequencing. OCT-4 gene expression and PIK3CA mutations were also clinically evaluated in BCa patients. The frequency of PIK3CA mutation in 44 new cases were 32%. PIK3CA mutations were significantly associated with HER2-positive (p = 0.0271) status, Ki-67 status (p = 0.0434) and patient age (p = 0.0149). OCT-4 mRNA expression was significantly higher in the BCa tissue in comparison to normal breast tissue (p = 0.0305). A significant correlation was found between expression of OCT-4 and node status (p = 0.0190). OCT-4 mRNA expression was higher in the PIK3CA mutation tissue than the wild type tissue. However, no association was found between the expression of OCT-4 and the PIK3CA mutation or wild type samples (p = 0.7908). Our results provided that OCT-4 gene and PIK3CA mutations may have a role in development of BCa. OCT-4 mRNA expression level and PIK3CA mutations have a potential important for BCa diagnosis or treatment.

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  AtıfScopus1·WoS1·OpenAlex1

  İncele
• MakaleAçık Erişim2017Scopus SJRQ2/r/bayburt/13619
  Comparison of telomere length and insulin-like growth factor-binding protein 7 promoter methylation between breast cancer tissues and adjacent normal tissues in Turkish women

  Kaya, Zehra; Akkiprik, Mustafa; Karabulut, Sevgi; Peker, Irem; Gullu Amuran, Gokce; Ozmen, Tolga; Gulluoglu, Bahadır M.; Kaya, Handan; Ozer, Ayse

  Background: Both insulin-like growth factor-binding protein 7 (IGFBP7) and telomere length (TL) are associated with proliferation and senescence of human breast cancer. This study assessed the clinical significance of both TL and IGFBP7 methylation status in breast cancer tissues compared with adjacent normal tissues. We also investigated whether IGFBP7 methylation status could be affecting TL. Methods: Telomere length was measured by quantitative PCR to compare tumors with their adjacent normal tissues. The IGFBP7 promoter methylation status was evaluated by methylation-specific PCR and its expression levels were determined by western blotting. Results: Telomeres were shorter in tumor tissues compared to controls (P<.0001). The mean TL was higher in breast cancer with invasive ductal carcinoma (IDC; n=72; P=.014) compared with other histological type (n=29), and TL in IDC with HER2 negative (n=53; P=.017) was higher than TL in IDC with HER2 positive (n=19). However, telomeres were shortened in advanced stages and growing tumors. IGFBP7 methylation was observed in 90% of tumor tissues and 59% of controls (P=.0002). Its frequency was significantly higher in IDC compared with invasive mixed carcinoma (IMC; P=.002) and it was not correlated either with protein expression or the other clinicopathological parameters. Conclusion: These results suggest that IGFBP7 promoter methylation and shorter TL in tumor compared with adjacent tissues may be predictive biomarkers for breast cancer. Telomere maintenance may be indicative of IDC and IDC with HER2 (−) of breast cancer. Further studies with larger number of cases are necessary to verify this association.

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  AtıfScopus6·WoS6·OpenAlex6

  İncele
• MakaleAçık Erişim2016Scopus SJRQ3/r/bayburt/13893
  Correlation between the DNA methylation and gene expression of IGFBP5 in breast cancer

  Karabulut, Sevgi; Kaya, Zehra; Amuran, Gökçe Gullu; Peker, Irem; Özmen, Tolga; Gulluolu, Bahadir M.; Kaya, Handan; Erzik, Can; Ozer, Ayşe; Akkiprik, Mustafa

  BACKGROUND: The insulin-like growth factor binding protein5 (IGFBP5) is often dysregulated in human cancers and considered neither a tumor suppressor nor an oncogene. OBJECTIVE: We aim to examine the reason of the changeable gene regulation of IGFBP5 in the case of methylation in breast cancer. METHODS: We used methyl-specific polymerase (MSP) chain reaction to detect CpG methylation of IGFBP5 promoter and exon-I in breast cancer and adjacent tissues. Gene expression is evaluated by quantative polymerase chain reaction (qPCR). RESULTS: IGFBP5 methylation was detected in 24 of 58 (41%) and 54 of 56 (96.5%) promoter and exon-I site respectively in tumor tissues. In adjacent tissues 17 of 58 (29%) and 53 of 56 (96.5%) was methylated. IGFBP5 expression was higher estrogene receptor (ER)(+) than ER(-) patients (p = 0:0549). Beside, we found a positive correlation between the expression of IGFBP5 and G2 tumor grade (p = 0:0131). However, no correlation was observed between IGFBP5 expression and age, menopause or the presence of lymph node metastasis (p > 0:05). CONCLUSIONS: In summary, our results showed that IGFBP5 promoter and exon-I methylation did not have any differences between tumor and adjacent tissues so that IGFBP5 methylation did not change IGFBP5 gene regulation in breast cancer. This is the first study investigating the IGFBP5 gene methylation in breast cancer.

  AtıfScopus9

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