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Introduction:Leptin (LEP) and LEP receptor (LEPR) play roles in cancer progression. We evaluated LEP-2548G/A and LEPR 668 A/G variants in patients with multiple myeloma (MM). In addition, the methylation status of CpG sites at 31 and 51 nucleotides (nt) according to the transcription start region of the LEPgene was examined.Methods:DNA was extracted from the peripheral blood of study participants who were healthy controls and patients with MM. These variants were analyzed using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. The methylation at -31 and -51 nt in the LEPwas performed using the methylation-specific PCR method. The 2-year progression-free survival (PFS) and 2-year overall survival (OS) were evaluated according to prognostic factors.Results:There was no significant difference in the genotype distributions of LEPR 668A/G and LEP-2548G/A between the control and patient groups (p>0.05). We found that -31 and -51 nt regions of the LEP gene were unmethylated in the patient group compared with the control group (p=0.051 and p=0.001, respectively). The -31 nt methylation was unchanged in 15 patients (78.94%). PFS and OS were higher in these patients than in the others. In multivariate analysis, the methylated/unmethylated ratio at -31 nt methylation was associated with a poor prognosis (p=0.020).Conclusion:To our knowledge, our study is the first to examine these variants and their methylation status in Turkish patients with MM. Our results showed that LEP gene -31 nt unmethylation was associated with PFS and OS. These results need to be confirmed in different ethnic and larger sample groups.

Objective: Mitochondria are multifunctional and dynamic organelles found in cells. Nicotine is a natural alkaloid found in the tobacco plant and has been well studied as a component of cigarette smoke. It has also been reported to affect mitochondrial function both in vitro and in vivo. Uncoupling protein 2 (UCP2) reduces generation of ROS by mitochondria. Our purpose in this study was to investigate whether the -866G/A variant of the UCP2 gene is associated with smoking status. Methods: A total of 238 individuals consisting of 138 smokers and 100 healthy controls were examined. The UCP2-866G/A variant was genotyped by polymerase chain reaction-restriction fragment length polymorphism method. Results: The proportion of individuals carrying the three possible genotype was significantly different between the smoker and healthy control groups. The UCP2-866G/A variant GG genotype was associated significantly with an increased risk of smoking (p=0.001) while AA genotype was associated significantly with a decreased risk of smoking (p=0.001). The UCP2-866G/A variant G allele was found to be increased in the smoker group compared to the healthy controls (p=0.001). Conclusion: Our data suggest that the UCP2-866 G/A variant GG genotype and G allele might reflect the risk of smoking status in a Turkish population.

Introduction: It has been shown that the host immune response and chronic inflammation could play a role as important risk factors for cancer. Oral squamous cell carcinoma (OSCC) is a common cancer worldwide. In this study, we aimed to evaluate the impact of interleukin-1 receptor antagonist (IL-1RA) and IL-4 variable number tandem repeat (VNTR) polymorphisms on OSCC susceptibility in a Turkish population. Methods: Study subjects comprised of 36 OSCC patients and 100 healthy controls. Genotyping of the IL-1RA VNTR (rs2234663) and IL-4 VNTR (rs79071878) polymorphisms were analyzed by polymerase chain reaction. Results: The frequency of IL-1RA VNTR 1/2+2/2 genotypes increased in the patients than healthy controls while IL-1RA VNTR 1/1 genotype was higher in the control group than in the patients (p=0.002). The subjects carrying IL-1RA VNTR 1/2+2/2 genotypes showed a 12.011-fold increased risk of susceptibility to OSCC. IL-1RA VNTR allele 1 was higher in the control group than the patient group while IL-1RA VNTR allele 2 was higher in the patient group than the control group (respectively, p=0.000, p=0.000). The subjects carrying IL-1RA VNTR allele 2 showed a 2.609-fold increased risk of susceptibility to OSCC. The IL-4 VNTR P1/P1 and P1/P2 genotype frequencies were higher in the patient group compared to the control group (p=0.039). IL-4 VNTR P1 allele was higher in the patients compared to the controls (p=0.030). Conclusion: The significant association between the functional VNTR polymorphisms of IL-1RA/IL-4 genes and OSCC suspectibility in a Turkish population confirmed a role of altered inflammatory process in OSCC pathogenesis.

Aim: To evaluate the susceptibility of the serotonin transporter-associated polymorphic region (5-HTTLPR) and complement factor H (CFH) gene variants to smoking status. Method: Smokers and non-smokers were included in the study. The smoking amount was assessed based on the scores on the Fagerström Test for Nicotine Dependence (FTND). DNA is extracted from blood samples. 5-HTTLPR and CFH Y402H variants were analyzed by polymerase chain reaction (PCR) and/or restriction fragment length polymorphism (RFLP) methods. The results were evaluated statistically. Results: 5-HTTLPR and CFH Y402H genotype and allele distribution did not differ significantly between smokers and non-smokers (p>0.05). There was no deviation from Hardy-Weinberg equilibrium (HWE) for these variants in the groups. Conclusion: Nicotine addiction is a complex phenomenon in which both genetic and environmental factors play a role. The identification of genes that play a role in addiction is important to elucidate the pathogenesis. The results of this study showed that 5-HTTLPR and CFH Y402H variants had no effect on nicotine addiction. However, these results need to be validated in larger sample groups and in different ethnic communities.

Background Multiple myeloma (MM) constitutes approximately 10% of hematological malignancies. Bisphosphonates have established themselves in solid organ metastasis and multiple myeloma lytic bone lesions by inhibiting osteoclast activation. Medication-related osteonecrosis of the jaw (MRONJ) emerges as an important complication. Investigating host-based factors, and developing personal risk factors gain importance in the development mechanism of MRONJ. We aimed to reveal the different genotype polymorphisms, and clinical effects of eNOS in patients with a diagnosis of MRONJ in MM patients. Methods Medical records and blood samples were collected from 60 MRONJ patients with MM and 60 healthy controls. Inclusion criteria was having an exposed maxillofacial bone for more than eight weeks, a history of bisphosphonates, and no history of radiation therapy for the jaws. eNOS G894T and intron 4 VNTR were calculated by polymerase chain reaction and/or restriction fragment length polymorphism. Results eNOS G894T and VNTR genotypes and alleles were compared statistically with the healthy control group. There was no significant difference between the two groups. In comparison between G894T and clinical parameters, aphthous stomatitis was more common in TT genotype, while DMFT > 3 was more common in TG-GG genotype ( p  = 0.035, 0.023). Conclusions eNOS induces osteogenesis in bone metabolism, with its regulatory effects on bone remodeling and also NO induced angiogenesis takes place indirectly with its protective effect on endothelial functions. We see that these polymorphisms affecting the entire process of bone remodeling and angiogenesis, especially mucosal damage, which is the triggering factor of MRONJ pathology, have been revealed in the MM patient group. Considering the MRONJ initiating factors, it is necessary to emphasize the importance of our study results. It should be seen as an important step for new studies towards MRONJ and its treatment.

Objective: The aim of the present study was to investigate any possible association between the macrophage migration inhibitory factor (MIF) –173GC variant and Behçet’s disease (BD) in a group of Turkish patients. Subjects and Methods: A total of 111 patients with BD and 100 healthy controls were enrolled in this study. Genomic DNA was extracted from peripheral lymphocytes. The MIF –173GC variant was genotyped using polymerase chain reaction restriction fragment length polymorphism. The allele and genotype frequencies of patients and controls were compared using the χ 2 test. Results: A statistically significant difference in the distribution of the genotype was observed between BD patients and healthy controls. The homo-genotype CC was more prevalent in the patient group compared to the control group (p = 0.008, OR: 0.24, 95% Cl: 0.05–0.78). A significant association was observed when the patients were compared with the controls according to GG + GC versus CC ge­notypes (p = 0.003, OR: 1.21, 95% CI: 0.06–0.063). Allele frequencies of the MIF −173GC variant did not show any statistically significant difference between patients and controls. Conclusion: In this study, we conclude that the CC ge­notype of the MIF –173GC variant may be a risk factor in the pathogenesis of BD in the Turkish population. However, further studies with larger samples are needed to address the exact role of this variant in BD.

OBJECTIVEOral squamous cell carcinoma (OSCC), with its low survival rates and increasing incidence, is due to various etiological factors including environmental, genetic, and epigenetic changes. Interleukin 6 (IL- 6) is a cytokine with both pro- and anti-inflammatory effects. Therefore, we investigated the possible association of the IL-6 gene variants with risk for OSCC in a Turkish cohort.METHODSThis study included 42 patients with OSCC and 110 age-and gender-matched healthy controls. Three variants (-174G/C [rs1800795], -572G/C (rs1800796), and -597G/A [rs1800797]) in the IL-6 promoter region were analyzed by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method.RESULTSThere was a significant difference in the genotype and allele frequencies of the IL-6 -174G/C variant between OSCC patients and controls. While the IL-6 -174G/C G/C genotype was higher in the patient group than in the control group, the G/G and C/C genotypes were lower in the patients compared to the control group (p=0.016, OR:0.653, 95% CI: 0.38-1.11). The genotype and allele distributions of -572G/C and -597G/A variants of the IL-6 gene were not statistically different between OSCC patients and the control group.CONCLUSIONOur current investigation is focused on the role of variants of IL-6 gene on OSCC. To the best of our knowledge, this study is the first study to evaluate the genotype and allele frequencies of IL-6 -174G/C, -572G/C, and 597G/A variants in patients with OSCC in a Turkish population. The results support that the IL-6 -174G/C variant may play an important role in susceptibility to OSCC in our population.

OBJECTIVE Oral squamous cell carcinoma (OSCC) is the most frequently seen oral malignancy and accounts for up to 80-90% of all malignant neoplasms that occurin the oral cavity. The p53 tumor suppressor gene plays a crucial role in the regulation of the cell cycle. Mutations of the p53 gene havean important role in OSCC carcinogenesis. In this study, we aimed to evaluate the C-deletion mutation in exon 4 codon 63 of p53 gene in Turkish patients with OSCC. METHODS A total of 60 subjects were enrolled in this study, 30 patients with a pathologic diagnosis of OSCC and 30 cases of age and sex-matched healthy controls. Genotyping was performed for all individuals using polymerase chain reaction (PCR) analysis. RESULTS The findings showed that the distribution of p53 exon 4 codon 63 C-deletion was significantly different between patient group and control group (p=0.000). It was detected that all patients had C-deletion mutation in exon 4 codon 63 of p53. CONCLUSION Our results suggest that C-deletion in exon 4 codon 63 deletion of the p53 gene may play a role in the pathogenesis of human OSCC in a Turkish cohort.

OBJECTIVE An increasing number of epidemiological and molecular evidence proposes that inflammation is a significant factor in the etiology of cancers. Macrophage Migration Inhibitory Factor (MIF) encodes a lymphokine involved in cell-mediated immunity, immunoregulation, and inflammation. It has been reported that MIF is linked with a higher risk of several cancer types. In the present study, we investigated the association of MIF rs755622 variant with the risk of breast cancer (BC) and gastrointestinal cancer in a Turkish cohort. METHODS The present study included a total of 153 subjects, which consisted of 33 BC patients, 53 gastrointestinal cancer patients and 67 healthy controls. Genomic DNA extracted from peripheral venous blood. The rs755622 variant of the MIF gene was genotyped using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. The results were statistically analyzed by calculating the odds ratios (OR) and 95% confidence intervals (CI) using the ?2 test. RESULTS There was a statistical difference between the BC patients and controls for the MIF rs755622 variant. MIF rs755622 GG genotype and G allele were increased in BC patients compared to controls (p=0.016, p=0.017, respectively). No significant difference was observed between gastrointestinal cancer patients and controls for the MIF rs755622 variant (p>0.05). CONCLUSION Our results showed that the MIF rs755622 variant might play a potential role in BC physiopathology.

OBJECTIVE Breast cancer (BC) is a heterogeneous malignancy and differs widely among different patients. The aim of this study was to investigate the relationship between the HER2/TOP2A gene aberrations and promoter methylation in RASSF1A/APC genes in patients with high-risk BC.METHODS Formalin-fixed paraffin embedded (FFPE) tissue samples from primary breast tumors (n=60) were assessed. HER2/TOP2A aberrations was evaluated using FISH method. DNA was extracted from FFPE tumor tissues, and Methylation-sensitive high resolution melting (MS-HRM) analysis were performed for RASSF1A/APC genes methylation status. RESULTS HER2 amplification and TOP2A aberration were observed in 15/60 (25%) and 18/60 (30%) cases, respectively. According to the statistical analysis, HER2 amplification was associated with higher tumor grade (p=0.001), PR status (p=0.025), and TOP2A aberrations (p=0.004). RASSF1A and APC methylation were 58/60 (96.6%) and 26/60 (43.3%), respectively. There was a significant correlation between APC methylation and TOP2A aberration. APC gene methylation was significantly more frequent in tumors with TOP2A aberration (p=0.026). CONCLUSION Our results suggested that APC gene promoter hypermethylation was associated with TOP2A gene aberrations in patients with high-risk BC. This may be significant for targeted individual therapy. Additionally, it was confirmed that there was significant association of TOP2A gene aberrations with the HER2 gene amplification seen in BC.