A Systematic Pan-Cancer Analysis of YY1 Aberrations and their Relationship with Clinical Outcome, Tumor Microenvironment, and Therapeutic Targets.

Yin-Yang 1 (YY1) has a crucial function in the development of several malignancies, according to recent research. However, nothing is known about its aberrant expression and prognostic significance in human pan-cancer. We first explored the potential carcinogenic effect of YY1 in 33 cancers using the cancer genome atlas (TCGA) project and gene expression omnibus (GEO) datasets in this research. Then, we contained a variety of elements, for instance, gene expression, the state of survival, gene alterations, protein phosphorylation, immune infiltration, and related cellular pathways, and used a series of bioinformatics methods to investigate the underlying molecular mechanism of YY1 in the etiology or clinical prognosis of various malignancies. In most malignancies, YY1 was expressed at high levels, and the level of YY1 expression was statistically associated with the prognosis of tumor patients. The S118 site of YY1 implied higher phosphorylation expression in breast cancer, colon cancer, uterine corpus endometrial carcinoma (UCEC), and lung adenocarcinoma (LUAD) tumor tissues, but lower phosphorylation levels in ovarian cancer and clear cell carcinoma tumor tissues. For S247, higher phosphorylation levels were found in colon cancer, UCEC, and LUAD tumor tissue, and lower phosphorylation expression was found in clear cell carcinoma tumor tissue. In TCGA database, YY1 expression in BRCA, BRCA-LumA, BRCA-LumB, CESC, CHOL, COAD, ESCA, HNSC, HNSC-HPV-, KIRP, LGG, LIHC, and PAAD tumor tissues was a statistically significant positive connection of the estimated infiltration value of cancer-associated fibroblasts but a negative correlation in TGCT. In addition, the functional mechanism of YY1 also involves viral carcinogenesis and ribonucleic acid (RNA) metabolism related functions. Our first pan-cancer analysis offers a pretty comprehensive knowledge of YY1's oncogenic involvement in various cancers.

Safety and efficacy of ultrasound-guided percutaneous thermal ablation in treating low-risk papillary thyroid microcarcinoma: A pilot and feasibility study.

OBJECTIVE: This study aimed to evaluate the safety and efficacy of thermal ablation in treating low-risk unifocal papillary thyroid microcarcinoma (PTMC). MATERIALS AND METHODS: Patients with unifocal PTMC were enrolled in this study, and thermal ablations were performed. Contrast-enhanced ultrasound was used to estimate the extent of ablation immediately after thermal ablation; complications were recorded. The size and volume of the ablated area and thyroid hormones were measured, and the clinical evaluations were performed at 1, 3, 6, 12, and 18 months after thermal ablation. From July 2016 to July 2017, the prospective study was conducted involving 107 patients. Thermal ablation was well tolerated without serious complications. RESULTS: Compared with the volume immediately after thermal ablation, the mean volume reduction ratio (VRR) of ablated lesions was 0.457 ± 0.218 (range: 0.040-0.979), 0.837 ± 0.150 (range: 0.259-1), 0.943 ± 0.090 (range: 0.491-1), 0.994-0.012 (range: 0.938-1), and 0.999 ± 0.002 (range: 0.992-1) at 1, 3, 6, 12, and 18 months after thermal ablation, respectively. Significant differences in the VRR were found between every two follow-up visits (P < 0.01). Results of patients' thyroid function test before thermal ablation and at 1 month after thermal ablation were normal, and no significant differences were observed (P > 0.05). No tumor regrowth, local recurrence, or distant metastases were detected during follow-up visits. CONCLUSION: Thermal ablation is a short-term safe and effective method in treating low-risk small PTMCs, which can be considered a potential alternative therapy for patients with PTMC.

Prospective analysis of tiopronin in prevention of sorafenib and antiviral therapy inducing liver toxicity in advanced hepatitis B virus-related hepatocellular carcinoma.

Hepatotoxicity induced by sorafenib and antiviral therapy is a limitation for its continuation treatment for patients with advanced hepatitis B virus-related hepatocellular carcinoma (HCC). This prospective study determined the efficacy of tiopronin in hepatotoxicity prevention of HBV-related HCC treatment. Eighty-two patients (median age, 50 years; 71 % male) of advanced HCC treated with sorafenib and antiviral therapy were included, of whom 40 were given the supplementation of tiopronin. The primary endpoint was liver function which was checked before the treatment and every week during the therapy. Besides, course discontinuations, dose reductions, HBV DNA levels and treatment efficacy were evaluated. Patient characteristics and liver function were comparable (p > 0.05). The proportion of abnormal liver function was significantly lower in tiopronin group than in control group including alanine transaminase (ALT, p = 0.035), aspartate aminotransferase (AST, p = 0.041), total bilirubin (TBIL, p = 0.021) and albumin (ALB, p = 0.001). Rates of course discontinuations (p = 0.024) and dose reductions (p = 0.046) were significantly lower in tiopronin groups, and disease control rate (p = 0.036) was higher. No difference was found in HBV DNA level. Multivariate regression analysis showed that sorafenib (OR 7.837; 95 % CI 3.845-15.333; p = 0.004), antiviral therapy (OR 3.871; 95 % CI 1.572-9.569; p = 0.044) and hepatoprotective drug (OR 3.007; 95 % CI 1.321-6.308; p = 0.046) played important roles in clinical outcome. Tiopronin tends to prevent the HCC patients from the treatment-induced hepatotoxicity, enhance patients' tolerance to sorafenib and antiviral therapy and even improve the cancer treatment efficacy.