The platform consists of three modules, which are pre‐configured bioinformatic pipelines, cloud toolsets, and online omics' courses. The pre‐configured bioinformatic pipelines not only combine analytic tools for metagenomics, genomes, transcriptome, proteomics and metabolomics, but also provide users with powerful and convenient interactive analysis reports, which allow them to analyze and mine data independently. As a useful supplement to the bioinformatics pipelines, a wide range of cloud toolsets can further meet the needs of users for daily biological data processing, statistics, and visualization. The rich online courses of multi‐omics also provide a state‐of‐art platform to researchers in interactive communication and knowledge sharing.

To gain mechanistic insights into the functions and developmental dynamics of tumor-infiltrated immune cells, especially B-lymphocytes, here we combine single-cell RNA-sequencing and antigen receptor lineage analysis to characterize a large number of triple-negative breast cancer infiltrated immune cells and report a comprehensive atlas of tumor-infiltrated B-lymphocytes. The single-cell transcriptional profiles reveal significant heterogeneity in tumor-infiltrated B-cell subgroups. The single-cell antigen receptor analyses demonstrate that compared with those in peripheral blood, tumor-infiltrated B-cells have more mature and memory B-cell characteristics, higher clonality, more class switching recombination and somatic hypermutations. Combined analyses suggest local differentiation of infiltrated memory B-cells within breast tumors. The B-cell signatures based on the single-cell RNA-sequencing results are significantly associated with improved survival in breast tumor patients. Functional analyses of tumor-infiltrated B-cell populations suggest that mechanistically, B-cell subgroups may contribute to immunosurveillance through various pathways. Further dissection of tumor-infiltrated B-cell populations will provide valuable clues for tumor immunotherapy.

Objective: To explore a new predictive model of lymphatic vascular infiltration (LVI) in rectal cancer based on magnetic resonance (MR) and computed tomography (CT). Methods: A retrospective study was conducted on 94 patients with histologically confirmed rectal cancer, they were randomly divided into training cohort (n = 65) and validation cohort (n = 29). All patients underwent MR and CT examination within 2 weeks before treatment. On each slice of the tumor, we delineated the volume of interest on T2-weighted imaging, diffusion weighted imaging, and enhanced CT images, respectively. A total of 1,188 radiological features were extracted from each patient. Then, we used the student t-test or Mann-Whitney U-test, Spearman's rank correlation and least absolute shrinkage and selection operator (LASSO) algorithm to select the strongest features to establish a single and multimodal logic model for predicting LVI. Receiver operating characteristic (ROC) curves and calibration curves were plotted to determine how well they explored LVI prediction performance in the training and validation cohorts. Results: An optimal multi-mode radiology nomogram for LVI estimation was established, which had significant predictive power in training (AUC, 0.884; 95% CI, 0.803-0.964) and validation (AUC, 0.876; 95% CI, 0.721-1.000). Calibration curve and decision curve analysis showed that the multimodal radiomics model provides greater clinical benefits. Conclusion: Multimodal (MR/CT) radiomics models can serve as an effective visual prognostic tool for predicting LVI in rectal cancer. It demonstrated great potential of preoperative prediction to improve treatment decisions.

The Src homology 2 domain-containing protein tyrosine phosphatase 2 (Shp2) is generally considered to be an oncogene owing to its ability in enhancing the malignancy of multiple types of tumor cells; however, its role in modulating tumor immunity remains largely elusive. Here, we reported that myeloid-restricted ablation of Shp2 suppressed melanoma growth. Mechanistically, loss of Shp2 potentiates macrophage production of CXCL9 in response to IFN-γ and tumor cell-derived cytokines, thereby facilitating the tumor infiltration of IFN-γ-producing T cells that could in turn support CXCL9 production within tumor microenvironment. Collectively, our findings highlight a causative role of myeloid Shp2 in dampening T cell-mediated antitumor immunity by restraining the macrophage/CXCL9-T cell/IFN-γ feedback loop. Thus, targeting macrophage Shp2 may help to create a Th1-dominant tumor immune microenvironment.

Dysregulation of microRNA plays critical roles in various malignancies. However, whether the aberrant expression of miR-215 in breast cancer is associated with malignancy, metastasis, or prognosis remains unknown. In this study, we demonstrated that the relative level of miR-215 expression was lower in cancer tissues compared with adjacent non-malignant tissues (p < 0.001). Low-miR-215 expression was observed to be closely correlated with higher tumor grade (p = 0.008), human epidermal growth factor receptor 2 (HER2) positivity (p = 0.006), HER2 positive breast cancer subtype (p = 0.016), and lymph node metastasis (p = 0.039). Moreover, patients with low-miR-215 expression showed shorter 5-year disease-specific survival (DSS) than the high-miR-215 expression group (p = 0.007). Multivariate analysis results revealed that miR-215 downexpression was an unfavorable prognostic factor for DSS in addition to tumor size, ER, and lymph node metastasis. Our results support the potential of miR-215 as a prognostic predictor for breast cancer with its high expression in cancer tissues and its relationship with other clinicopathologic factors and survival.