In the sample set, a positive correlation between HNF1B and ECI2 protein expression was detected (P=0.005). HNF1B mRNA was also positively correlated with HNF1B protein expression (P=0.001). HNF1B promoter methylation was detected in 26/67 (38.8%) of cases. A novel pathogenic somatic HNF1B mutation was detected in 1/61 (1.6%) of the analysed HGSC cases. No other correlations between the examined SNPs (rs4430796, rs757210 and rs7405776), HNF1B promoter methylation, HNF1B/ECI2 expression or clinicopathological characteristics were found.Esophageal cancer is one of the most common types of malignancy worldwide. At present, surgical resection is the main treatment for esophageal cancer, but recurrence and distant metastasis are the main causes of mortality. The transcription factors Twist, Slug and Snail regulate epithelial-mesenchymal transition and thereby participate in tumor invasion and metastasis. selleck The aim of the present study was to investigate the expression of Twist, Slug and Snail in esophageal squamous cell carcinoma (ESCC) and their prognostic significance. The expression of Twist, Slug and Snail in 229 paraffin-embedded ESCC and matched normal mucosal tissues was detected by immunohistochemistry. The expression differences of Twist, Slug and Snail in the ESCC and normal tissues were compared by χ2 test, and the associations between the three proteins and the clinicopathological parameters of ESCC were analyzed. The expression levels of Twist, Slug and Snail in 29 fresh frozen ESCC and matched normal mucosal tissues were detected byaled that Snail influenced the overall survival, as did the co-expression of Twist and Snail. Nerve invasion was also identified as an independent factor affecting the progression-free survival of ESCC. The results indicate that Twist is highly expressed, Slug may be a tumor suppressor, and Snail is an independent prognostic factor in ESCC. Twist and Snail are positively correlated, and the simultaneous inhibition of Twist and Snail protein expression may be beneficial for prolonging the overall survival of patients with ESCC.Choline kinase (ChK) catalyzes the first step in the CDP-choline pathway for the synthesis of phosphatidylcholine. The α isoform of this enzyme is overexpressed in various types of cancer and its inhibition or downregulation has been applied as an anticancer strategy. In spite of increasing attention being paid to ChK expression, as well as its activity and inhibition in cancer, there are only limited studies available on the regulation of ChK, including its regulation by microRNAs (miRNAs/miRs). The dysregulation of gene expression by miRNAs is a common cause for carcinogenesis. In the present study, miR-367-3p was predicted to target the 3′-untranslated region (UTR) of the ChK α (chka) mRNA transcript. The binding of miR-367-3p to the 3′-UTR of chka was validated by a luciferase assay. The effects of the miR-367-3p mimic on chka gene and protein expression levels were determined by reverse transcription-quantitative polymerase chain reaction and western blot analysis, respectively. miR-367-3p significantly downregulated the expression of chka to ~60% of the negative control. Cells transfected with miR-367-3p exhibited higher levels of apoptosis and a lower cell migration compared with the control. To the best of our knowledge, the present study provided the first experimental evidence of the regulation of chka expression by miR-367-3p. The pro-apoptotic and suppressive effects of miR-367-3p on cell migration were similar to the anticancer effects resulting from the inhibition of ChK enzyme activity or the knockdown of chka gene expression by small interfering RNA. Therefore, these findings may potentially lead to the use of miR-367-3p in anticancer strategies that target ChK.Follicular dendritic cell sarcoma (FDCS) is an extremely rare tumor, which mainly originates from FDCs in the lymph nodes. Sometimes FDCS can arise from outside the lymph nodes due to the existence of acquired lymphoid tissue, which becomes the histological basis of the tumor. The diagnosis of FDCS, particularly extranodal FDCS, presents a challenge for pathologists and hematopathologists. The present study presents two cases of extranodal FDCS based on clinical features and histomorphology. Soft tissue of the chest wall was involved in case 1 and right tonsil tissue in case 2. Case 1 underwent surgery, and was in good health post-operatively. During the 5-month post-operative follow-up period, the patient was healthy in all respects. Case 2 received surgery combined with radiotherapy, and the follow-up data reported that the patient remained alive, without signs of recurrence or metastasis during the 4-month post-operative follow-up period. Additionally, a total of 102 cases of extranodal FDCS were retrieved from the literature, which were extracted and reviewed carefully. The rates of recurrence, metastasis and mortality were 14.63 (12/82), 17.07 (14/82) and 8.29% (15/82), respectively. The overall survival rates of the 102 cases, showing 2-year total survival rates, were 70%, the same with that of 5-year total survival rates. The 2-year tumor-free total survival rates were 68%, and the 5-year equivalents were 32%. Female patients had a poorer prognosis than male patients (P0.05).Numerous factors can affect the quality of oocytes; however, the effects of cancer on the quality of oocytes and the underlying mechanisms remain unclear. In the present study, the effects of the sarcoma-180 (S-180) cell line on the quality of oocytes were investigated using S-180 tumor-bearing mice. In total, 42 female C57BL/6J mice were randomly divided into the tumor-bearing group and the control group, with 21 mice per group. The weight of the mice and ovaries were recorded, and blood glucose, serum insulin, lipopolysaccharide, triglyceride (TG) and total cholesterol (TC) levels were analyzed using the corresponding detection kits. Hematoxylin and eosin staining was performed to observe the pathological changes of the ovarian tissue, and reverse transcription-quantitative PCR (RT-qPCR) was used to analyze the expression levels of meiosis arrest female 1 (MARF1), SUMO-specific protease 7 (SENP7), aralkylamine N-acetyltransferase (AANAT), cell division cycle 25B and glycine-rich protein 3. The results of the present study revealed that the number of oocytes in the two groups of mice was similar; however, the number of abnormal oocytes was increased in the tumor-bearing group.