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Background: Colorectal polyp is known a precursor of colorectal cancer (CRC) that holds an increased risk for progression to CRC. Circulating cell-free DNA (cfDNA) methylation has shown favorable performance in the detection and monitoring the malignant progression in a variety of cancers. Results: To discover cfDNA methylation markers for the diagnosis of CRC, we first performed a genome-wide analysis between eight CRC and eight polyp tissues using the Infinium HumanMethylationEPIC BeadChip. We identified 7008 DMCs, and after filtering, we validated 39 DMCs by MethylTarget sequencing in 62 CRC and 56 polyp tissues. A panel of four CpGs (cg04486886, cg06712559, cg13539460, and cg27541454) was selected as the methylation marker in tissue by LASSO and random forest models. A diagnosis prediction model was built based on the four CpGs, and the methylation diagnosis score (md-score) can effectively discriminate tissues with CRC from polyp patients (AUROC > 0.9). Finally, the cg27541454 was confirmed hypermethylated in CRC (AUC = 0.85) in the plasma validation cohort. Conclusions: Our findings suggest that the md-score could robustly detect CRC from polyp tissues, and cg27541454 may be a promising candidate noninvasive biomarker for CRC early diagnosis. [ABSTRACT FROM AUTHOR]

Aims/Introduction To investigate the association between two single nucleotide polymorphisms ( SNPs; rs3774261 and rs822393) in the ADIPOQ gene and type 2 diabetes mellitus in Han Chinese from northeast China. Materials and Methods The present study comprised 993 type 2 diabetes mellitus patients and 966 unrelated controls from northeastern China. Two SNPs were sequenced using SNPscan. The distribution of genotype frequencies of the two SNPs in ADIPOQ between cases and controls, and in subgroups stratified based on body mass index, were compared using logistic regression analysis. Linear regression was used to analyze the association between each SNP and clinical indicators. Results The GG genotype of rs3774261 increased the risk of type 2 diabetes mellitus compared with the AA genotype in participants with a body mass index <24 ( P = 0.021; odds ratio 1.636, 95% CI 1.708-2.484). Rs822393 was correlated with glycosylated hemoglobin ( P = 0.043) in controls. Rs3774261 had an association with diastolic blood pressure ( P = 0.017) in controls, and in controls with a body mass index <24; rs3774261 also had an association with both systolic blood pressure ( P = 0.025) and diastolic blood pressure ( P = 0.043). Conclusions The present results confirm the association between ADIPOQ variants and type 2 diabetes mellitus in northeastern China. However, additional larger replication studies are required to validate these findings. [ABSTRACT FROM AUTHOR]

Introduction: PTC is not generally considered a lethal disease, but prone to recurrence as the prognosis. Hashimoto's thyroiditis (HT) is an important factor that affects the prognosis of papillary thyroid carcinoma (PTC). It is crucial to find biomarkers to identify the combination of HT with PTC and to predict the prognosis. Methods: RNASeq data from the Cancer Genome Atlas (TCGA) database was used to screen differentially expressed genes (DEGs) of PTC with HT via the edgeR package of R software version 3.3.0. Also, the DEGs were applied to the DAVID web-based tool to determine the enrichment of gene functions via Gene Ontology (GO) analysis and to identify associated pathways in the Kyoto Encyclopedia of Genes and Genomes (KEGG) database. By constructing protein interaction networks within Cytoscape software, we screened candidate genes and explored possible relationships with the clinical phenotype of PTC. Finally, additional thyroid tissue samples were collected to verify the results above. Results: After analyzing the RNA-Seq data of PTC patients from the Cancer Genomic Atlas, 497 differentially expressed PTC genes were found to be associated with HT, of which protein tyrosine phosphatase receptor type C (PTPRC), KIT, and COL1A1 were associated with tumor size and lymph node metastasis (p < 0.05). Verification of these results with another 30 thyroid tissues of clinical PTC patients revealed that the expression level of PTPRC in the PTC with HT group was higher than that in the PTC without HT group (p < 0.05) and the ROC curve showed a good discrimination (area under the curve = 0.846). However, the correlation with the clinical phenotype was not statistically significant (p > 0.05). Discussion: These data suggest that upregulation of PTPRC enhances the incidence of HT associated with PTC and is also predictive of a poor prognosis. [ABSTRACT FROM AUTHOR]

The aim of this study was to examine the impact of iodine on the development of thyroid cancer cells and to detect the underlying mechanisms. It was observed that proliferation was promoted and apoptosis was inhibited in cells treated with iodine at a specific concentration. This treatment group was then selected for further analysis, to investigate how iodine affects the development of thyroid cancer cells. It was reported that sperm protein associated with the nucleus, X-linked, family member A1 (SPANXA1) expression in iodine-treated cells was significantly upregulated. Furthermore, downregulation of SPANXA1 inhibited cell proliferation, migration and invasion, and promoted cell apoptosis. These results suggested that SPANXA1 played an important role in iodine-treated thyroid cancer cells. Novel associations between SPANXA1 and thyroid cancer were described in the current study. In addition, SPANXA1 gene silencing resulted in the downregulation of PI3K and phosphorylated (p)AKT expression in iodine-treated thyroid cancer cells, whereas iodine treatment alone resulted in upregulated PI3K and p-AKT expression. Inhibiting PI3K further suppressed cell proliferation and contributed to apoptosis, even in the presence of SPANXA1 at high levels. As a consequence, PI3K/AKT may be one of the key signalling pathways by which iodine promotes thyroid cancer development in association with SPANXA1. In addition, our results further suggested that patients with thyroid cancer may need to avoid high-iodine intake. [ABSTRACT FROM AUTHOR]