Objectives: To evaluate the efficacy and treatment-related toxicity of accelerated hyperfractionation field-involved re-irradiation combined with concurrent capecitabine chemotherapy for locally recurrent and irresectable rectal cancer (LRIRC). Methods: 72 patients with LRIRC who underwent the treatment were studied. Threedimensional conformal accelerated hyperfractionation radiotherapy (3D-CAHRT) was performed and the dose was delivered with a schedule of 1.2 Gy twice daily, with an interval of at least 6 h between fractions, 5 days a week. Concurrent capecitabine chemotherapy was administered twice daily. After 36 Gy in 30 fractions over 3 weeks, patients were evaluated to define the resectability of the disease. If resection was not feasible irradiation was resumed until the total dose administered to the tumour reached 51.6-56.4 Gy. Results: Two patients temporarily interrupted concurrent chemoradiation because of Grade IV diarrhoea. The remaining 70 patients completed the planned concurrent chemoradiation. In all patients, the complete response rate was 8.3% and the partial response rate was 51.4%. The overall response rate was 59.7% and clinical benefit rate was 93.1%. Symptomatic responses proved to be obvious and tumour resection was performed in 18 patients. The overall median survival time and median progressionfree survival time were 32 and 17 months, respectively. 3 year overall survival and progression-free survival were 45.12% and 31.19%, respectively. Severely acute toxicities included Grade III-IV diarrhoea and granulocytopenia with 9.7% and 8.3% incidence respectively. Small bowel obstruction was severely late toxicity, and the incidence was 1.4%. Conclusion: Three-dimensional conformal accelerated hyperfractionation fieldinvolved re-irradiation combined with concurrent capecitabine chemotherapy might be an effective and well-tolerated regimen for patients with LRIRC.

Identification of modules in molecular networks is at the core of many current analysis methods in biomedical research. However, how well different approaches identify disease-relevant modules in different types of gene and protein networks remains poorly understood. We launched the “Disease Module Identification DREAM Challenge”, an open competition to comprehensively assess module identification methods across diverse protein-protein interaction, signaling, gene co-expression, homology, and cancer-gene networks. Predicted network modules were tested for association with complex traits and diseases using a unique collection of 180 genome-wide association studies (GWAS). Our critical assessment of 75 contributed module identification methods reveals novel top-performing algorithms, which recover complementary trait-associated modules. We find that most of these modules correspond to core disease-relevant pathways, which often comprise therapeutic targets and correctly prioritize candidate disease genes. This community challenge establishes benchmarks, tools and guidelines for molecular network analysis to study human disease biology (https://synapse.org/modulechallenge).

Background: Renal cell carcinoma is one of the most common and lethal types of cancer within the urinary system. the current challenges include how to diagnose RCC in the earlier stage and the drug resistance to chemotherapy or radiotherapy. Therefore, to investigate the survival rate and immune infiltration in RCC base on gene expression of IFI16 in RCC. Methods: We explored the relationship between the transcription level of IFI16 and clinical data in RCC through various online databases, including ONCOMINE, GEPIA, Timer and COEXPEDIA. Results: In comparison with the corresponding normal tissues, the mRNA expression levels of IFI16 are higher in KIRC tissues (p＜ 0.05), while lower in KICH tissues (p＜0.05). The mRNA expression of IFI16 has a positive correlation with TNM stage in KIRC(p=8.56e-07) and KIRP(p=0.00078). In KIRC, the higher expression of IFI16 suggests lower OS（HR=1.4; P=0.037; Log-rank p=0.037). In KIRP, the higher expression of IFI16 suggests lower DFS and OS (respectively, HR=1.9, P=0.037, Log-rank p=0.034; HR=2.3, P=0.011, Log-rank p=0.0091). In contrast, the expression level of IFI16 has a negative correlation with the tumour purity in KICH, KIRC and KIRP via the Timer database (all, p < 0.05). In KIRC and KIRP, the expression level of IFI16 has a positive correlation with the tumor-infiltrating immune cells (TIICs) (all, p < 0.05), except the macrophages in KIRP. In KIRC, the main TIICs in the arm-level deletion state of the IFI16 gene were B cell, CD4+T cell, Neutrophil, and Dendritic cell, while the main TIICs in the high amplification state were Macrophage (all, p < 0.0001). 108 genes are co-expressed with the IFI16 gene. Function enrichment analysis by GO and KEGG mainly enriched on some functions, including neutrophil degranulation, phagocytosis, vesicle-mediated transport regulation and enriched on some signal pathways, including tuberculosis, toxoplasmosis, phagosome, leishmaniasis, and Fc gamma R-med8ted. Conclusions: IFI16 acts as an oncogene in the progression of kidney cancer which is overexpressed in the RCC tissues. Apart from that, IFI16 has been determined as a marker of diagnosis and prognosis in RCC, which might be associated with the immune infiltration.