Type 2 diabetes has been shown to occur in response to environmental and genetic influences, among them nutrition, food intake patterns, sedentary lifestyle, body mass index (BMI), and exposure to persistent organic pollutants (POPs), such as polychlorinated biphenyls (PCBs). Nutrition is essential in the prevention and management of type 2 diabetes and has been shown to modulate the toxicity of PCBs. Serum carotenoid concentrations, considered a reliable biomarker of fruit and vegetable intake, are associated with the reduced probability of chronic diseases, such as type 2 diabetes and cardiovascular disease. Our hypothesis is that fruit and vegetable intake, reflected by serum carotenoid concentrations, is associated with the reduced probability of developing type 2 diabetes in US adults with elevated serum concentrations of PCBs 118, 126, and 153. This cross-sectional study utilized the CDC database, National Health and Nutrition Examination Survey (NHANES) 2003–2004 in logistic regression analyses. Overall prevalence of type 2 diabetes was approximately 11.6% depending on the specific PCB. All three PCBs were positively associated with the probability of type 2 diabetes. For participants at higher PCB percentiles (e.g., 75th and 90th) for PCB 118 and 126, increasing serum carotenoid concentrations were associated with a smaller probability of type 2 diabetes. Fruit and vegetable intake, as reflected by serum carotenoid concentrations, predicted notably reduced probability of dioxin-like PCB-associated risk for type 2 diabetes.
Gastric cancer is one of the lethal causes of cancer-related deaths worldwide. The incidence and mortality rates of this disease is comparatively higher in China. In the current study, we evaluated the anticancer effects of Thymoquinone (TQ) against gastric cancer cells (MGC80-3 and SGC-7901) and normal noncancerous GES-1 cells and attempted to investigate the underlying mechanism. Our results indicated that TQ exhibited significant growth inhibitory effects on gastric cancer cells (MGC80-3 and SGC-7901). However, lower cytotoxicity was observed against normal GES-1 cells. Moreover, TQ could inhibit the colony formation potential of MGC80-3 and SGC-7901 cells in a dose-dependent manner. TQ also inhibited cell migration ability of the gastric cancer cells and down-regulated the expression of the mesenchymal genes such as , and TWIST. However, the epithelial markers such as E-cadherin and cytokeratin-19 were distinctly up-regulated in TQ-treated gastric cancer cells. Since PI3K/Akt/ mTOR plays an important role in progression and tumorigenesis, we also investigated the effect of TQ on PI3K/Akt/mTOR signalling pathway in gastric cancer cells. It was observed that TQ down-regulated the expression of some of the key proteins of this pathway. Taken together, we conclude that TQ may prove lead molecule for the treatment of gastric cancer.
Objectives
The levels of tumor markers in pancreatic neuroendocrine carcinoma (PNEC) are unknown, and imaging findings of PNEC and pancreatic ductal adenocarcinoma (PDAC) have overlaps. In this study, we show the tumor markers in PNEC and evaluate their values for distinguishing PNEC from PDAC.
Methods
Thirty-three cases of PDAC and 21 cases of PNEC were retrospectively evaluated. The demographic information and clinical data were reviewed.
Results
Pancreatic neuroendocrine carcinoma was usually misdiagnosed (57.1%) as PDAC based on imaging findings. Abnormal carbohydrate antigen (CA) 19-9, carcinoembryonic antigen (CEA), and α-fetoprotein (AFP) were observed in 19.0% to 28.6% of PNECs. Abnormal CA 19-9 and CA 125 levels were more common in PDAC than in PNEC (P < 0.05). Higher level of AFP was more common in PNEC than in PDAC (33.3% vs 3.0%, P < 0.05). The cutoff value of CA 19-9 for detecting PNEC was calculated as 38.5 U/mL or less with 0.788 sensitivity and 0.800 specificity. Carbohydrate antigen 19-9 (odds ratio [OR], 22.9; 95% confidence interval [CI], 2.94–179.3), AFP (OR, 0.08; 95% CI, 0.012–0.564), and CA 125 (OR, 17.4; 95% CI, 1.13–267.3) were predictors in differentiating PDAC from PNEC.
Conclusions
Carbohydrate antigen 19-9, AFP, and CA 125 have potential for distinguishing hypovascularized PNEC from PDAC.
Background: The outcomes of ovarian cancer patients are very poor, therefore it is necessary to find prognostic biomarkers and explore the potential underlying molecular mechanisms of ovarian cancer.Methods: In this study, a gene expression microarray data set covering 562 ovarian serous cystadenocarcinomas and 12,042 genes was downloaded from The Cancer Genome Atlas (TCGA) database.For each candidate gene, samples were allocated into a "high group" or a "low group" according to the expression level. The overall survival (OS) rates were compared between the two groups. Then, a univariate analysis and a multivariate Cox proportional hazards test were carried out to examine the associations between genes and multiple clinicopathological parameters.Results: Among all candidate genes, PI3 (peptidase inhibitor 3, often called elafin) and HLA-DOB (major histocompatibility complex, class II, DO beta) were identified as hub genes. PI3 (P=7.99e-7) and HLA-DOB (P=7.52e-6) showed significant associations with OS, especially in patients with stage III or IV disease.Both PI3 (HR =1.84, P=3.77e-7) and HLA-DOB (HR =0.68, P=0.001134) were identified as independent predictors of ovarian cancer patients OS. In addition, IRF1 (interferon regulatory factor 1) (P=1.16e-15) and SPI1 (Spi-1 proto-oncogene) (P=2.03e-6) were identified as the most significant transcription factors.
Conclusions:Our data indicate that PI3 and HLA-DOB are potential biomarkers that could be used to predict the prognosis of ovarian cancer patients, and may play important roles in ovarian cancer progression.Further experimental and clinical studies with larger sample sizes are needed to confirm these findings.
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