N⁶-methyladenosine (m⁶A), the most abundant modification in eukaryotic cells, regulates RNA transcription, processing, splicing, degradation, and translation. Circular RNA (circRNA) is a class of covalently closed RNA molecules characterized by universality, diversity, stability and conservatism of evolution. Accumulating evidence shows that both m⁶A modification and circRNAs participate in the pathogenesis of multiple diseases, such as cancers, neurological diseases, autoimmune diseases, and infertility. Recently, m⁶A modification has been identified for its enrichment and vital biological functions in regulating circRNAs. In this review, we summarize the role of m⁶A modification in the regulation and function of circRNAs. Moreover, we discuss the potential applications and possible future directions in the field.

Thyroid cancer is rapidly increasing in incidence worldwide in the past several decades, same as the incidence of metabolic syndrome. We performed a system review and meta-analysis of the association between metabolic syndrome, its components and insulin resistance and thyroid cancer incidence. We searched several computer-assisted databases PUBMED, EMBASE and ISI Web of Science to identify studies published before 31st January 2018. Every study must report either risk estimates of thyroid cancer incidence with 95% confidence interval (CI) or related data can speculate. Two investigators independently identified eligible studies and extracted data. Evaluating the summaries of relative risk estimates use both fixed and random effects methods. We found 42 articles met the inclusion criteria of this review. There is an increased risk for thyroid cancer for patients with insulin resistance (relative risk [RR] = 1.59, 95%confidence interval [CI] = 1.12-2.27, P = 0.01), dysglycemia (RR = 1.40, 95%CI = 1.15-1.70,P < 0.001), high BMI (RR = 1.35,95%CI = 1.23-1.48,P < 0.001) and hypertension(RR = 1.34,95%CI = 1.22-1.47, p < 0.001). However, patients with dyslipidemia, both total cholesterol (RR = 1.09, 95%CI = 0.98-1.21, P = 0.13) and triglyceride (RR = 1.01, 95%CI = 0.91-1.12, P = 0.82) was not associated with thyroid cancer. Our meta-analysis showed Insulin Resistance, dysglycemia, high BMI and hypertension significantly increased the thyroid cancer risk. These results may help identify people with high risk of thyroid cancer and change to healthy life style.

Metformin, as the preferred antihyperglycemic drug for type 2 diabetes, has been found to have a significant effect in inhibiting tumor growth in recent years. However, metformin alone in cancer treatment has the disadvantages of high dose concentrations and few targeted cancer types. Increasing studies have confirmed that metformin can be used in combination with conventional anticancer therapy to obtain more promising clinical benefits, which is expected to be rapidly transformed and applied in clinic. Some combination therapy strategies including metformin combined with chemotherapy, radiotherapy, targeted therapy and immunotherapy have been proven to have more significant antitumor effects and longer survival time than monotherapy. In this review, we summarize the synergistic antitumor effects and mechanisms of metformin in combination with other current conventional anticancer therapies. In addition, we update the research progress and the latest prospect of the metformin-combined application in the cancer treatment. This work could provide more evidence and future direction for the clinical application of metformin in antitumor.

Background: It is widely accepted that maximal extrathyroidal extension (ETE) plays a vital role in the prognosis of papillary thyroid carcinoma (PTC). However, there is no consensus among researchers about the meaning of minimal ETE (mETE) in PTC. Herein, we conducted a systematic review and meta-analysis to examine the role of mETE in the prognosis of PTC. Methods: We searched PubMed, EMBASE, and Cochrane search trials databases in English to identify studies comparing data on disease recurrence in PTC patients with mETE and those with no ETE. To summarize the data related to mETE status, risk ratios and hazard ratios adjusted for potential confounders were used to assess the number of recurrence and time-dependent risks related to mETE status, respectively . Results: According to the inclusion criteria, a total of 7951 patients from 9 studies were included. The recurrence rate in patients with mETE is significantly higher when compared with those with no ETE (risk ratio = 1.70, 95% confidence interval: 1.26–2.28, I ² = 56%). According to the data summarized with hazard ratios , PTC patients with mETE showed a significantly increased risk of disease recurrence. Conclusion: mETE is a risk factor for poor prognosis in patients with PTC. Our innovative classification of ETE has its value in assessing the prognosis of PTC.

Isocitrate dehydrogenase (IDH) is a key metabolic enzyme catalyzing the interconversion of isocitrate to α-ketoglutarate (α-KG). Mutations in IDH lead to loss of normal enzymatic activity and gain of neomorphic activity that irreversibly converts α-KG to 2-hydroxyglutarate (2-HG), which can competitively inhibit a-KG-dependent enzymes, subsequently induces cell metabolic reprograming, inhibits cell differentiation, and initiates cell tumorigenesis. Encouragingly, this phenomenon can be reversed by specific small molecule inhibitors of IDH mutation. At present, small molecular inhibitors of IDH1 and IDH2 mutant have been developed, and promising progress has been made in preclinical and clinical development, showing encouraging results in patients with IDH2 mutant cancers. This review will focus on the biological roles of IDH2 mutation in tumorigenesis, and provide a proof-of-principle for the development and application of IDH2 mutant inhibitors for human cancer treatment.