This study aimed to construct a model for using in differentiating benign and malignant nodules with the artificial neural network and to increase the objective diagnostic accuracy of US. 618 consecutive patients (528 women, 161 men) with 689 thyroid nodules (425 malignant and 264 benign nodules) were enrolled in the present study. The presence and absence of each sonographic feature was assessed for each nodule - shape, margin, echogenicity, internal composition, presence of calcifications, peripheral halo and vascularity on color Doppler. The variables meet the following criteria: important sonographic features and statistically significant difference were selected as the input layer to build the ANN for predicting the malignancy of nodules. Six sonographic features including shape (Taller than wide, p<0.001), margin (Not Well-circumscribed, p<0.001), echogenicity (Hypoechogenicity, p<0.001), internal composition (Solid, p<0.001), presence of calcifications (Microcalcification, p<0.001) and peripheral halo (Absent, p<0.001) were significantly associated with malignant nodules. A three-layer 6-8-1 feed-forward ANN model was built. In the training cohort, the accuracy of the ANN in predicting malignancy of thyroid nodules was 82.3% (AUROC = 0.818), the sensitivity and specificity was 84.5% and 79.1%, respectively. In the validation cohort, the accuracy, sensitivity and specificity was 83.1%, 83.8% and 81.8%, respectively. The AUROC was 0.828. ANN constructed by sonographic features can discriminate benign and malignant thyroid nodules with high diagnostic accuracy.

The anti-tumor effects of S-allylcysteine (SAC), a water-soluble garlic derivative, on human ovarian cancer cells have been previous studied in vitro and in vivo models but the precise epigenetic molecular mechanisms are still unclear. This study aimed to investigate the epigenetic mechanism of SAC. Human epithelial ovarian cancer cell line A2780 was selected. Cell proliferation and cell cycle was analyzed. DNA methylation, DNA methyltransferase (DNMT) activity, tumor suppressor gene expressions, as well as protein expression were analyzed. SAC could inhibit the proliferation of A2780 cells in dose- and time-dependent manners (the IC50 was 16.25 mmol/L and 5.25 mmol/L at 48 h and 72 h). Treatment of A2780 cells with SAC resulted in G1/S phase arrest. SAC treatment decreased global DNA methylation levels in A2780 cells in a dose-dependent manner. SAC decreased the levels of 5-methylcytosine, DNMT activity, messenger RNA (mRNA) and protein levels of DNMT1. Additionally, SAC treatment resulted in re-expression of the mRNA and proteins of silenced tumor suppressor gene CDKN1A accompany with reduced cell division control 2 expression. Our data indicated the potential therapeutic effects of SAC on the human ovarian carcinoma cell line A2780 in vitro. The epigenetic mechanism of action of SAC may have important implications for epigenetic therapy.

Introduction: Plasma circulating tumor DNA (ctDNA) is an ideal approach to detecting the epidermal growth factor receptor ( EGFR ) T790M mutation, which is a major mechanism of resistance to first‐generation EGFR‐tyrosine kinase inhibitor (TKI) therapy. The present study aimed to explore the association of ctDNA‐identified T790M mutation with disease failure sites and clinical prognosis in non‐small cell lung cancer (NSCLC) patients. Methods: Patients who progressed on first‐generation TKIs were categorized into failure site groups of chest limited (CF), brain limited (BF) and other (OF). Amplification refractory mutation system (ARMS) and droplet digital PCR (ddPCR) were used to identify the T790M mutation in ctDNA. Prognosis was analyzed with Kaplan–Meier methods. Results: Overall concordance between the two methods was 78.3%. According to both ARMS and ddPCR, patients in the OF group had a significantly higher rate of T790M mutation than did patients in the BF and CF groups ( P < 0.001), and a significantly higher T790M mutation rate was also observed in OF‐group patients than in those in the CF and BF groups ( P < 0.001). AZD9291 was found to be an excellent treatment option and yielded the longest survival for T790M+ patients in all groups who had progressed on EGFR‐TKIs; for other treatments, the prognosis of T790M− patient subgroups varied. Conclusions: The present study demonstrates that T790M mutation in ctDNA is associated with failure sites for NSCLC patients after EGFR‐TKI therapy and indicates that both failure site and T790M mutational status greatly influence treatment selection and prognosis.

For many decades, lung cancer has been the most common cancer and the leading cause of cancer death worldwide. More than 50% of non-small-cell lung cancer patients receive radiotherapy (alone or in combination with chemotherapy or surgery) during their treatment. The intrinsic radiosensitivity of tumors and dose-limiting toxicity restrict the curative potential of radiotherapy. Histone deacetylase inhibitors (HDACis) are an emerging class of agents that target histone deacetylase and represent promising radiosensitizers that affect various biological processes, such as cell growth, apoptosis, DNA repair, and terminal differentiation. Histone deacetylase inhibitors have been found to suppress many important DNA damage responses by downregulating proteins in the homologous recombination and nonhomologous end joining repair pathways in vitro. In this review, we describe the rationale for using HDACis as radiosensitizers and the clinical evidence regarding the use of HDACis for the treatment of non-small-cell lung cancer.