The new aspect of oncometabolite can be an indicator of genetic and epigenetic change and cancer biomarker.

Blood test is a kind of liquid biopsy that checks cancer cells or cancer nucleic acids circulating freely from cells in the blood. A liquid biopsy may be used to distinguish cancer at early stages and it could be a game-changer for both cancer diagnosis and prognosis strategies. Liquid biopsy tests consider several tumor components, such as DNA, RNA, proteins, and the tiny vesicles originating from tumor cells. Actually, liquid biopsy signifies the genetic alterations of tumors through nucleic acids or cells in various body fluids, including blood, urine, cerebrospinal fluid, or saliva in a noninvasive manner. In this review, we present an overall description of liquid biopsy in which circulating tumor cells, cell-free nucleic acids, exosomes, and extrachromosomal circular DNA are included.

Promoter methylation in a number of tumor-suppressor genes (TSGs) can play crucial roles in the development of thyroid carcinogenesis. The focus of the current meta-analysis was to determine the impact of promoter methylation of eight selected candidate TSGs on thyroid cancer and to identify the most important molecules in this carcinogenesis pathway. A comprehensive search was performed using Pub Med, Scopus, and ISI Web of Knowledge databases, and eligible studies were included. The methodological quality of the included studies was evaluated according to the Newcastle Ottawa scale table and pooled odds ratios (ORs); 95% confidence intervals (CIs) were used to estimate the strength of the associations with Stata 12.0 software. Egger’s and Begg’s tests were applied to detect publication bias, in addition to the “Metatrim” method. A total of 55 articles were selected, and 135 genes with altered promoter methylation were found. Finally, we included eight TSGs that were found in more than four studies (RASSF1, TSHR, PTEN, SLC5A, DAPK, P16, RARβ2, and CDH1). The order of the pooled ORs for these eight TSGs from more to less significant was CDH1 (OR = 6.73), SLC5 (OR = 6.15), RASSF1 (OR = 4.16), PTEN (OR = 3.61), DAPK (OR = 3.51), P16 (OR = 3.31), TSHR (OR = 2.93), and RARβ2 (OR = 1.50). Analyses of publication bias and sensitivity confirmed that there was very little bias. Thus, our findings showed that CDH1 and SCL5A8 genes were associated with the risk of thyroid tumor genesis.

Thyroid cancer is a frequent endocrine related malignancy with continuous increasing incidence. There has been moving development in understanding its molecular pathogenesis recently mainly through the explanation of the original role of several key signaling pathways and related molecular distributors. Central to these mechanisms are the genetic and epigenetic alterations in these pathways, such as mutation and DNA rearrangements. That does not mean, however, that all the somatic abnormalities here in a cancer genome have been involved in development of the cancer and just driver mutations are concerned in tumor initiation. By way of illustrations, MAPK pathway which is motivated by BRAFV600E and RAS and RET / PTC rearrangements are suggesting driver genetic alterations in follicular derived thyroid cancers which are considered in this review.