Is there a Relationship Between Caffeine Intake and Smoking and Positive and Negative Symptom Severity in Schizophrenia?

BACKGROUND: It has been reported that caffeine intake and smoking are more frequent in patients with schizophrenia than the general population. However, the cause of high caffeine and smoking and its correlation with positive and negative symptoms is unclear. Therefore, the aim of the present study is to evaluate the correlation between daily caffeine intake and smoking and the severity of positive and negative symptoms in patients with schizophrenia. SUBJECTS AND METHODS: This study included 177 participants, 89 of whom were healthy controls and 88 patients with schizophrenia. Scale for the Assessment of Positive Symptoms (SAPS) and Scale for the Assessment of Negative Symptoms (SANS) scales were applied to the patients with schizophrenia to measure the severity of positive and negative symptoms of the disease. RESULTS: The amounts of caffeine and tobacco consumption were significantly higher in the patients group than healthy controls (p=0.001 and p<0.001, respectively). There was no significant correlations between daily caffeine consumption and SAPS or SANS scores in patients with schizophrenia. There was a significant positive relationship between SAPS-delusions score and tobacco consumption. CONCLUSIONS: Our study is the first study in the literature that examines the relationship between caffeine and cigarette intake and SANS and SAPS scales in patients with schizophrenia. Although caffeine intake is higher in patients with schizophrenia than healthy controls, this study is valuable as it shows that it is not associated with symptom severity. In addition, although it is known that smoking is high in patients with schizophrenia, this study showed a positive relationship between SAPS-delusion scores and tobacco consumption.

CT120: A New Potential Target for c-Myc in Head and Neck Cancers.

Background: CT120 is a universally expressed protein with seven transmembrane domains. It functions in cell proliferation, survival and apoptosis by activating Raf/MEK/ERK and PI3K/Akt signaling pathways. Evidence suggests that CT120 plays important roles in lung carcinogenesis and oncogenic pathway activation. c-Myc is an important transcription factor modulating cell progression, apoptosis and cellular transformation. Previous studies have shown that MYC gene is amplified in many types of cancer including head and neck squamous cell carcinoma (HNSCC). Myc can regulate expression of many genes by binding to E-boxes. The aim of this study was to investigate the relationship between c-Myc protein and CT120 gene. Methods: Tumor and normal tissue samples from 50 patients with HNSCC were investigated with chromatin immunoprecipitation assay (ChIP), Illumina MiSeq, bisulphite sequencing and qRT-PCR. Results: c-Myc binds to all E-boxes except E-box 5 on CT120 promoter. The CpG dinucleotides were found to be partially methylated in all tumor and normal tissue samples. Bisulphite sequencing showed a 10% down-regulation in the methylation levels of the tumor tissues. CT120 gene was hypomethylated and up-regulated in 56% of the tumor tissue samples. Expression of c-Myc was significantly higher in tumor tissues than in non-cancerous tissue samples. MYC was overexpressed in 68% of the tumor tissue samples compared to normal tissues. The mean MYC levels were 2.42-fold higher in the tumor tissue samples. In 48% of the tumor tissues, MYC and CT120A mRNA were up- or down-regulated simultaneously (p<0.001). Conclusion: We show that CT120 gene is a target of c-Myc and it contributes to cancer progression in HNSCC.

CT120A Acts as an Oncogene in Head and Neck Squamous Cell Carcinoma.

Squamous cell carcinoma of the head and neck (HNSCC) is among the most frequent cancers worldwide. The etiology and pathogenesis of HNSCC are influenced by multiple genetic factors in addition to environmental and lifestyle-related factors. However, the mechanism underlying the HNSCC is still far from clear. The membrane associated gene CT120 was previously identified from chromosome 17p13.3 as a lung cancer-associated gene. Its function as an activator of the Erk and Akt signaling pathways in human lung cancer cell lines suggested that CT120 has an oncogenic function. However, there is no data in the literature on the role of CT120 in any other cancer type. Therefore, the aim of this study was to determine the expression rate and probable function of CT120 in HNSCC. Tumor tissues from 50 patients were analyzed by real-time quantitative RT-PCR to investigate the expression rate and by direct sequencing to differentiate the CT120A and CT120B variants. CT120 overexpression was observed in 58% of tumors compared to non-cancerous tissue samples and this up-regulation was directly associated with the upregulation of the CT120A variant and with the stage of the disease (p=0.001). Our results indicate that the CT120 gene may function in the development of HNSCC.

DLEC1 is not silenced solely by promoter methylation in head and neck squamous cell carcinoma.

Different types of genetic and epigenetic changes are associated with HNSCC. The molecular mechanisms of HNSCC carcinogenesis are still undergoing intensive investigation. The Deleted in lung and esophageal cancer 1 (DLEC1) gene is frequently silenced by methylation in various kinds of cancer. However, there is no data in the literature investigating the DLEC1 gene in the HNSCC. Tumor tissues from 97 patients were analyzed by real-time quantitative RT-PCR and DLEC1 expression levels were correlated with the methylation of the DLEC1 gene promoter. A statistically significant down-regulation was observed in tumors compared to non-cancerous tissue samples (p = 0.00). However, this down-regulation was not directly associated with hypermethylation of the promoter (p ≥ 0.05). Our results indicate that the DLEC1 gene may play an important role in the development of HNSCC. However, its down-regulation is not associated with the clinicopathological parameters and is not solely under the control of promoter methylation.