Screening ANLN and ASPM as bladder urothelial carcinoma-related biomarkers based on weighted gene co-expression network analysis.

Introduction: Bladder cancer (BLCA) is one of the most common malignancies in the urinary system with a poor prognosis and high treatment costs. Identifying potential prognostic biomarkers is significant for exploring new therapeutic and predictive targets of BLCA. Methods: In this study, we screened differentially expressed genes using the GSE37815 dataset. We then performed a weighted gene co-expression network analysis (WGCNA) to identify the genes correlated with the histologic grade and T stage of BLCA using the GSE32548 dataset. Subsequently, Kaplan Meier survival analysis and Cox regression were used to further identify prognosis-related hub genes using the datasets GSE13507 and TCGA-BLCA. Moreover, we detected the expression of the hub genes in 35 paired samples, including BLCA and paracancerous tissue, from the Shantou Central Hospital by qRT-polymerase chain reaction. Results: This study showed that Anillin (ANLN) and Abnormal spindle-like microcephaly-associated gene (ASPM) were prognostic biomarkers for BLCA. High expression of ANLN and ASPM was associated with poor overall survival.The qRT-PCR results revealed that ANLN and ASPM genes were upregulated in BLCA, and there was a correlation between the expression of ANLN and ASPM in cancer tissues and paracancerous tissue. Additionally, the increasing multiples in the ANLN gene was obvious in high-grade BLCA. Discussion: In summary, this preliminary exploration indicated a correlation between ANLN and ASPM expression. These two genes, serving as the risk factors for BLCA progression, might be promising targets to improve the occurrence and progression of BLCA.

Influencing factors for mortality in prostate cancer patients with T1 and T2 stage: a retrospective cohort study.

Background: Few reports have focused on the influencing factors of localized prostate cancer (PCa)-specific mortality so far. This study aimed to develop a competitive risk model for identifying the factors influencing the localized PCa mortality rate based on 135,310 subjects in the Surveillance, Epidemiology, and End Results (SEER) database. Methods: We included 135,310 localized PCa male patients from SEER database 2004-2016 in this cohort study, and collected the baseline information of all patients, including age of diagnosis, race, marital status, socioeconomic status (SES), American Joint Committee on Cancer (AJCC) stage, prostate-specific antigen (PSA) Gleason score, and so on. The outcome was considered as PCa-specific mortality in this study. The end time of follow-up was November 2018. Independent risk factors were examined by multivariate Fine-Gray analysis. The results are shown by hazard ratio (HR) and 95% confidence interval (CI). Results: All patients were divided into three groups: died from localized PCa (n=1,400), died from other causes (n=16,996), and survived (n=116,914). The diagnostic age of 119,899 patients was ≥55 years. The multivariate Fine-Gray analysis indicated that age of diagnosis (55-70 years: HR =1.473, 95% CI: 1.124-1.930; >70 years: HR =2.528, 95% CI: 1.901-3.362), race (American India/Alaska Native, Asian/Pacific Islander: HR =0.653, 95% CI: 0.490-0.870), marital status (divorced: HR =1.433, 95% CI: 1.197-1.717; single: HR =1.463, 95% CI: 1.244-1.719; widowed: HR =1.485, 95% CI: 1.222-1.804), therapeutic method (radiotherapy: HR =1.500; 95% CI: 1.119-2.011), SES (4-10: HR =0.799, 95% CI: 0.664-0.961; ≥11: HR =0.670; 95% CI: 0.534-0.839), AJCC stage (HR =0.820, 95% CI: 0.715-0.940), level of PSA (HR: 1.002, 95% CI: 1.002-1.002) and Gleason score (HR: 2.226, 95% CI: 2.108-2.350) were associated with the risk of localized PCa mortality. Conclusions: The study determined the influencing factors for mortality in patients with localized PCa through a competitive risk model. This finding may provide a reference for localized PCa patients: localized PCa patients who are older, divorced, widowed, single, have a radiotherapy, have a high PSA level, and Gleason score may be at high risk.

Molecular mapping of quantitative disease resistance loci for soybean partial resistance to Phytophthora sansomeana.

KEY MESSAGE: Two soybean QDRL were identified with additive interaction to P. sansomeana isolate MPS17-22. Further analyses uncovered four interaction patterns between the two QDRL and seven additional P. sansomeana isolates. Phytophthora sansomeana is a recently recognized species that contributes to root rot in soybean. Previous studies indicated that P. sansomeana is widely distributed among soybean growing regions and has a much wider host range than P. sojae, a well-known pathogen of soybean. Unlike P. sojae, no known disease resistance genes have been documented that can effectively control P. sansomeana. Therefore, it is important to identify resistance that can be quickly integrated into future soybean varieties. E13901 is an improved soybean line that confers partial resistance to P. sansomeana. A mapping population of 228 F4:5 families was developed from a cross between E13901 and a susceptible improved soybean variety E13390. Using a composite interval mapping method, two quantitative disease resistance loci (QDRL) were identified on Chromosomes 5 (designated qPsan5.1) and 16 (designated qPsan16.1), respectively. qPsan5.1 was mapped at 54.71 cM between Gm05_32565157_T_C and Gm05_32327497_T_C. qPsan5.1 was contributed by E13390 and explained about 6% of the disease resistance variation. qPsan16.1 was located at 39.01 cM between Gm16_35700223_G_T and Gm16_35933600/ Gm16_35816475. qPsan16.1 was from E13901 and could explain 5.5% of partial disease resistance. Further analysis indicated an additive interaction of qPsan5.1 and qPsan16.1 against P. sansomeana isolate MPS17-22. Marker assisted resistance spectrum analysis and progeny tests verified the two QDRL and their interaction patterns with other P. sansomeana isolates. Both QDRL can be quickly integrated into soybean varieties using marker assisted selection.

Long non-coding RNA SNHG14 contributes to gastric cancer development through targeting miR-145/SOX9 axis.

This study aimed to elucidate the roles of long non-coding RNA SNHG14 in gastric cancer development. LncRNA SNHG14 was markedly up-regulated in gastric cancer tissues and cells. Knockdown of SNHG14 significantly inhibited SGC-7901 cell viability, migration, invasion, and promoted cell apoptosis. In addition, miR-145 was negatively regulated by SNHG14 and the effects of SNHG14 knockdown on cell viability, apoptosis, migration, invasion, and the expression of apoptosis-related proteins and EMT-markers were reversed by inhibition of miR-145 at the same time. Furthermore, SOX9 was verified as a functional target of miR-145, and miR-145 regulated tumor malignant behaviors through regulating SOX9. Besides, knockdown of SNHG14 inhibited the expression of p-PI3 K, p-AKT, and p-mTOR and promoted PTEN expression, where miR-145 inhibition had opposite effects. Moreover, the activated PI3 K/AKT/mTOR pathway caused by miR-145 inhibition was counteracted after knockdown of SOX9. Our findings indicate that up-regulation of lncRNA SNHG14 may contribute to gastric cancer development via targeting miR-145/SOX9 axis and involving in PI3 K/AKT/mTOR pathway. SNHG14-miR-145/SOX9 axis may be a promising therapeutic strategy for gastric cancer treatment.

Genetic polymorphisms in TNIP1 increase the risk of gastric carcinoma.

The distribution and levels of TNIP1 in malignant and normal gastric mucosa are different, but it is not known whether TNIP1 polymorphisms are related to gastric carcinogenesis. To assess the association between four TNIP1 SNPs (rs3792792, rs4958881, rs7708392, rs10036748) and carcinogenesis, we used Sequenom Mass-ARRAY technology to determine the genotypes of 302 gastric carcinoma patients and 300 healthy controls in a Northwest Chinese Han population. These data were then compared using the Chi-square test/Fisher's exact test, genetic model analysis, and haplotype analysis. Odds ratios (OR) and 95% confidence intervals (CI) were used to evaluate the correlation. We observed that patients with the "G" allele of rs7708392 and the "C" allele of rs10036748 showed an increased risk of gastric carcinoma (OR= 1.335, 95%CI: 1.021-1.745, P= 0.035; OR= 1.358, 95%CI: 1.039-1.774, P= 0.025, respectively). Conversely, the haplotype "CT" of TNIP1 (rs7708392-rs10036748) may act as a genetic protective factor for gastric carcinoma (adjusted OR= 0.731, 95%CI: 0.552-0.970, P= 0.030). Our results are the first to suggest that genetic variation in TNIP1 gene is associated with gastric carcinoma, though, this finding must be confirmed in other populations with larger sample size.

Application of Thoracoscopic Hybrid Surgery in the Treatment of Stage III Tuberculous Empyema.

BACKGROUND: To investigate the efficacy and value of thoracoscopic hybrid surgery in the treatment of stage III chronic tuberculous empyema (CTE). METHODS: 48 patients diagnosed as CTE with pleural thickening and encysted abscess cavity from were treated by hybrid operation (HO). Small incision operation was first used for resection of thickening pleural fibreboard and decortication of parietal pleura. Then, thoracoscopy was guided into chest to decorticate the visceral pleurali. Additional 25 patients with open operation of pleurectomy were set as control. RESULTS: The average operation time of HO group was 70 ± 22 min compared to 130 ± 32 min of control. The amount of bleeding, hospitalization time and chest tube drainage of HO group (200 ± 55 ml, 18 ± 1.2 days, 3.5 ± 1.5 days) were significantly decreased compared to control (400 ± 45 ml, 28 ± 4.5 days, 6.5 ± 2.5 days). Post operation complications occurred in 5 (10.42%) and 3 (12%) cases for HO group and control, respectively. CONCLUSIONS: In stage III CTE, the small incision assisted thoracoscopic hybrid surgery help to remove thickening parietal pleura, promote the application of thoracoscopy, which has obvious advantages compared to traditional surgery.