BACKGROUND: As single-cell genomics experiments increase in complexity and scale, the need to integrate multiple datasets has grown. Such integration enhances cellular feature identification by leveraging larger data volumes. However, batch effects-technical variations arising from differences in labs, times, or protocols-pose a significant challenge. Despite numerous proposed batch correction methods, many still have limitations, such as outputting only dimension-reduced data, relying on computationally intensive models, or resulting in overcorrection for batches with diverse cell type composition. RESULTS: We introduce a novel method for batch effect correction named SCITUNA, a Single-Cell data Integration Tool Using Network Alignment. We perform evaluations on 39 individual batches from four real datasets and a simulated dataset, which include both scRNA-seq and scATAC-seq datasets, spanning multiple organisms and tissues. A thorough comparison of existing batch correction methods using 13 metrics reveals that SCITUNA outperforms current approaches and is successful at preserving biological signals present in the original data. In particular, SCITUNA shows a better performance than the current methods in all the comparisons except for the multiple batch integration of the lung dataset where the difference is 0.004. CONCLUSION: SCITUNA effectively removes batch effects while retaining the biological signals present in the data. Our extensive experiments reveal that SCITUNA will be a valuable tool for diverse integration tasks.

MOTIVATION: A major challenge in cancer genomics is to distinguish the driver mutations that are causally linked to cancer from passenger mutations that do not contribute to cancer development. The majority of existing methods provide a single driver gene list for the entire cohort of patients. However, since mutation profiles of patients from the same cancer type show a high degree of heterogeneity, a more ideal approach is to identify patient-specific drivers. RESULTS: We propose a novel method that integrates genomic data, biological pathways and protein connectivity information for personalized identification of driver genes. The method is formulated on a personalized bipartite graph for each patient. Our approach provides a personalized ranking of the mutated genes of a patient based on the sum of weighted 'pairwise pathway coverage' scores across all the samples, where appropriate pairwise patient similarity scores are used as weights to normalize these coverage scores. We compare our method against five state-of-the-art patient-specific cancer gene prioritization methods. The comparisons are with respect to a novel evaluation method that takes into account the personalized nature of the problem. We show that our approach outperforms the existing alternatives for both the TCGA and the cell line data. In addition, we show that the KEGG/Reactome pathways enriched in our ranked genes and those that are enriched in cell lines' reference sets overlap significantly when compared to the overlaps achieved by the rankings of the alternative methods. Our findings can provide valuable information toward the development of personalized treatments and therapies. AVAILABILITY AND IMPLEMENTATION: All the codes and data are available at https://github.com/abu-compbio/PersonaDrive, and the data underlying this article are available in Zenodo, at https://doi.org/10.5281/zenodo.6520187. SUPPLEMENTARY INFORMATION: Supplementary data are available at Bioinformatics online.

BACKGROUND: Recent cancer genomic studies have generated detailed molecular data on a large number of cancer patients. A key remaining problem in cancer genomics is the identification of driver genes. RESULTS: We propose BetweenNet, a computational approach that integrates genomic data with a protein-protein interaction network to identify cancer driver genes. BetweenNet utilizes a measure based on betweenness centrality on patient specific networks to identify the so-called outlier genes that correspond to dysregulated genes for each patient. Setting up the relationship between the mutated genes and the outliers through a bipartite graph, it employs a random-walk process on the graph, which provides the final prioritization of the mutated genes. We compare BetweenNet against state-of-the art cancer gene prioritization methods on lung, breast, and pan-cancer datasets. CONCLUSIONS: Our evaluations show that BetweenNet is better at recovering known cancer genes based on multiple reference databases. Additionally, we show that the GO terms and the reference pathways enriched in BetweenNet ranked genes and those that are enriched in known cancer genes overlap significantly when compared to the overlaps achieved by the rankings of the alternative methods.

SUMMARY: Long non-coding RNAs (lncRNAs) can act as molecular sponge or decoys for an RNA-binding protein (RBP) through their RBP-binding sites, thereby modulating the expression of all target genes of the corresponding RBP of interest. Here, we present a web tool named RBPSponge to explore lncRNAs based on their potential to act as a sponge for an RBP of interest. RBPSponge identifies the occurrences of RBP-binding sites and CLIP peaks on lncRNAs, and enables users to run statistical analyses to investigate the regulatory network between lncRNAs, RBPs and targets of RBPs. AVAILABILITY AND IMPLEMENTATION: The web server is available at https://www.RBPSponge.com. SUPPLEMENTARY INFORMATION: Supplementary data are available at Bioinformatics online.