Showing 106 of total 106 results (show query)

bioc

Moonlight2R:Identify oncogenes and tumor suppressor genes from omics data

The understanding of cancer mechanism requires the identification of genes playing a role in the development of the pathology and the characterization of their role (notably oncogenes and tumor suppressors). We present an updated version of the R/bioconductor package called MoonlightR, namely Moonlight2R, which returns a list of candidate driver genes for specific cancer types on the basis of omics data integration. The Moonlight framework contains a primary layer where gene expression data and information about biological processes are integrated to predict genes called oncogenic mediators, divided into putative tumor suppressors and putative oncogenes. This is done through functional enrichment analyses, gene regulatory networks and upstream regulator analyses to score the importance of well-known biological processes with respect to the studied cancer type. By evaluating the effect of the oncogenic mediators on biological processes or through random forests, the primary layer predicts two putative roles for the oncogenic mediators: i) tumor suppressor genes (TSGs) and ii) oncogenes (OCGs). As gene expression data alone is not enough to explain the deregulation of the genes, a second layer of evidence is needed. We have automated the integration of a secondary mutational layer through new functionalities in Moonlight2R. These functionalities analyze mutations in the cancer cohort and classifies these into driver and passenger mutations using the driver mutation prediction tool, CScape-somatic. Those oncogenic mediators with at least one driver mutation are retained as the driver genes. As a consequence, this methodology does not only identify genes playing a dual role (e.g. TSG in one cancer type and OCG in another) but also helps in elucidating the biological processes underlying their specific roles. In particular, Moonlight2R can be used to discover OCGs and TSGs in the same cancer type. This may for instance help in answering the question whether some genes change role between early stages (I, II) and late stages (III, IV). In the future, this analysis could be useful to determine the causes of different resistances to chemotherapeutic treatments. An additional mechanistic layer evaluates if there are mutations affecting the protein stability of the transcription factors (TFs) of the TSGs and OCGs, as that may have an effect on the expression of the genes.

Maintained by Matteo Tiberti. Last updated 2 months ago.

dnamethylationdifferentialmethylationgeneregulationgeneexpressionmethylationarraydifferentialexpressionpathwaysnetworksurvivalgenesetenrichmentnetworkenrichment

25.2 match 5 stars 6.59 score 43 scripts

bioc

MoonlightR:Identify oncogenes and tumor suppressor genes from omics data

Motivation: The understanding of cancer mechanism requires the identification of genes playing a role in the development of the pathology and the characterization of their role (notably oncogenes and tumor suppressors). Results: We present an R/bioconductor package called MoonlightR which returns a list of candidate driver genes for specific cancer types on the basis of TCGA expression data. The method first infers gene regulatory networks and then carries out a functional enrichment analysis (FEA) (implementing an upstream regulator analysis, URA) to score the importance of well-known biological processes with respect to the studied cancer type. Eventually, by means of random forests, MoonlightR predicts two specific roles for the candidate driver genes: i) tumor suppressor genes (TSGs) and ii) oncogenes (OCGs). As a consequence, this methodology does not only identify genes playing a dual role (e.g. TSG in one cancer type and OCG in another) but also helps in elucidating the biological processes underlying their specific roles. In particular, MoonlightR can be used to discover OCGs and TSGs in the same cancer type. This may help in answering the question whether some genes change role between early stages (I, II) and late stages (III, IV) in breast cancer. In the future, this analysis could be useful to determine the causes of different resistances to chemotherapeutic treatments.

Maintained by Matteo Tiberti. Last updated 5 months ago.

dnamethylationdifferentialmethylationgeneregulationgeneexpressionmethylationarraydifferentialexpressionpathwaysnetworksurvivalgenesetenrichmentnetworkenrichment

11.0 match 17 stars 6.57 score

bioc

mixOmics:Omics Data Integration Project

Multivariate methods are well suited to large omics data sets where the number of variables (e.g. genes, proteins, metabolites) is much larger than the number of samples (patients, cells, mice). They have the appealing properties of reducing the dimension of the data by using instrumental variables (components), which are defined as combinations of all variables. Those components are then used to produce useful graphical outputs that enable better understanding of the relationships and correlation structures between the different data sets that are integrated. mixOmics offers a wide range of multivariate methods for the exploration and integration of biological datasets with a particular focus on variable selection. The package proposes several sparse multivariate models we have developed to identify the key variables that are highly correlated, and/or explain the biological outcome of interest. The data that can be analysed with mixOmics may come from high throughput sequencing technologies, such as omics data (transcriptomics, metabolomics, proteomics, metagenomics etc) but also beyond the realm of omics (e.g. spectral imaging). The methods implemented in mixOmics can also handle missing values without having to delete entire rows with missing data. A non exhaustive list of methods include variants of generalised Canonical Correlation Analysis, sparse Partial Least Squares and sparse Discriminant Analysis. Recently we implemented integrative methods to combine multiple data sets: N-integration with variants of Generalised Canonical Correlation Analysis and P-integration with variants of multi-group Partial Least Squares.

Maintained by Eva Hamrud. Last updated 5 days ago.

immunooncologymicroarraysequencingmetabolomicsmetagenomicsproteomicsgenepredictionmultiplecomparisonclassificationregressionbioconductorgenomicsgenomics-datagenomics-visualizationmultivariate-analysismultivariate-statisticsomicsr-pkgr-project

4.7 match 182 stars 13.71 score 1.3k scripts 22 dependents

bioc

NoRCE:NoRCE: Noncoding RNA Sets Cis Annotation and Enrichment

While some non-coding RNAs (ncRNAs) are assigned critical regulatory roles, most remain functionally uncharacterized. This presents a challenge whenever an interesting set of ncRNAs needs to be analyzed in a functional context. Transcripts located close-by on the genome are often regulated together. This genomic proximity on the sequence can hint to a functional association. We present a tool, NoRCE, that performs cis enrichment analysis for a given set of ncRNAs. Enrichment is carried out using the functional annotations of the coding genes located proximal to the input ncRNAs. Other biologically relevant information such as topologically associating domain (TAD) boundaries, co-expression patterns, and miRNA target prediction information can be incorporated to conduct a richer enrichment analysis. To this end, NoRCE includes several relevant datasets as part of its data repository, including cell-line specific TAD boundaries, functional gene sets, and expression data for coding & ncRNAs specific to cancer. Additionally, the users can utilize custom data files in their investigation. Enrichment results can be retrieved in a tabular format or visualized in several different ways. NoRCE is currently available for the following species: human, mouse, rat, zebrafish, fruit fly, worm, and yeast.

Maintained by Gulden Olgun. Last updated 5 months ago.

biologicalquestiondifferentialexpressiongenomeannotationgenesetenrichmentgenetargetgenomeassemblygo

12.2 match 1 stars 4.60 score 6 scripts

bioc

SCANVIS:SCANVIS - a tool for SCoring, ANnotating and VISualizing splice junctions

SCANVIS is a set of annotation-dependent tools for analyzing splice junctions and their read support as predetermined by an alignment tool of choice (for example, STAR aligner). SCANVIS assesses each junction's relative read support (RRS) by relating to the context of local split reads aligning to annotated transcripts. SCANVIS also annotates each splice junction by indicating whether the junction is supported by annotation or not, and if not, what type of junction it is (e.g. exon skipping, alternative 5' or 3' events, Novel Exons). Unannotated junctions are also futher annotated by indicating whether it induces a frame shift or not. SCANVIS includes a visualization function to generate static sashimi-style plots depicting relative read support and number of split reads using arc thickness and arc heights, making it easy for users to spot well-supported junctions. These plots also clearly delineate unannotated junctions from annotated ones using designated color schemes, and users can also highlight splice junctions of choice. Variants and/or a read profile are also incoroporated into the plot if the user supplies variants in bed format and/or the BAM file. One further feature of the visualization function is that users can submit multiple samples of a certain disease or cohort to generate a single plot - this occurs via a "merge" function wherein junction details over multiple samples are merged to generate a single sashimi plot, which is useful when contrasting cohorots (eg. disease vs control).

Maintained by Phaedra Agius. Last updated 5 months ago.

softwareresearchfieldtranscriptomicsworkflowstepannotationvisualization

13.0 match 4.00 score 2 scripts

md-anderson-bioinformatics

NGCHMDemoData:Demo Data for the NGCHM R Package

Package of demo data for NGCHM vignettes.

Maintained by Mary A Rohrdanz. Last updated 9 months ago.

20.5 match 2.20 score 16 scripts

ccicb

CRUX:Easily explore patterns of somatic variation in cancer using 'CRUX'

Shiny app for exploring somatic variation in cancer. Powered by maftools.

Maintained by Sam El-Kamand. Last updated 1 years ago.

9.8 match 2 stars 2.00 score 5 scripts

ccicb

TCGAgistic:Easily access TCGA gistic data

Streams TCGA GISTIC2 copynumber data into the R session.

Maintained by Sam El-Kamand. Last updated 2 years ago.

5.4 match 5 stars 2.88 score 8 scripts 1 dependents

bioc

RESOLVE:RESOLVE: An R package for the efficient analysis of mutational signatures from cancer genomes

Cancer is a genetic disease caused by somatic mutations in genes controlling key biological functions such as cellular growth and division. Such mutations may arise both through cell-intrinsic and exogenous processes, generating characteristic mutational patterns over the genome named mutational signatures. The study of mutational signatures have become a standard component of modern genomics studies, since it can reveal which (environmental and endogenous) mutagenic processes are active in a tumor, and may highlight markers for therapeutic response. Mutational signatures computational analysis presents many pitfalls. First, the task of determining the number of signatures is very complex and depends on heuristics. Second, several signatures have no clear etiology, casting doubt on them being computational artifacts rather than due to mutagenic processes. Last, approaches for signatures assignment are greatly influenced by the set of signatures used for the analysis. To overcome these limitations, we developed RESOLVE (Robust EStimation Of mutationaL signatures Via rEgularization), a framework that allows the efficient extraction and assignment of mutational signatures. RESOLVE implements a novel algorithm that enables (i) the efficient extraction, (ii) exposure estimation, and (iii) confidence assessment during the computational inference of mutational signatures.

Maintained by Luca De Sano. Last updated 5 months ago.

biomedicalinformaticssomaticmutation

3.3 match 1 stars 4.60 score 3 scripts

michaelklein916

crso:Cancer Rule Set Optimization ('crso')

An algorithm for identifying candidate driver combinations in cancer. CRSO is based on a theoretical model of cancer in which a cancer rule is defined to be a collection of two or more events (i.e., alterations) that are minimally sufficient to cause cancer. A cancer rule set is a set of cancer rules that collectively are assumed to account for all of ways to cause cancer in the population. In CRSO every event is designated explicitly as a passenger or driver within each patient. Each event is associated with a patient-specific, event-specific passenger penalty, reflecting how unlikely the event would have happened by chance, i.e., as a passenger. CRSO evaluates each rule set by assigning all samples to a rule in the rule set, or to the null rule, and then calculating the total statistical penalty from all unassigned event. CRSO uses a three phase procedure find the best rule set of fixed size K for a range of Ks. A core rule set is then identified from among the best rule sets of size K as the rule set that best balances rule set size and statistical penalty. Users should consult the 'crso' vignette for an example walk through of a full CRSO run. The full description, of the CRSO algorithm is presented in: Klein MI, Cannataro V, Townsend J, Stern DF and Zhao H. "Identifying combinations of cancer driver in individual patients." BioRxiv 674234 [Preprint]. June 19, 2019. <doi:10.1101/674234>. Please cite this article if you use 'crso'.

Maintained by Michael Klein. Last updated 6 years ago.

3.3 match 2.32 score 21 scripts

kaiaragaki

classifyBLCA:What the Package Does (One Line, Title Case)

What the package does (one paragraph).

Maintained by Kai Aragaki. Last updated 2 years ago.

3.8 match 1.70 score

bioc

MatrixQCvis:Shiny-based interactive data-quality exploration for omics data

Data quality assessment is an integral part of preparatory data analysis to ensure sound biological information retrieval. We present here the MatrixQCvis package, which provides shiny-based interactive visualization of data quality metrics at the per-sample and per-feature level. It is broadly applicable to quantitative omics data types that come in matrix-like format (features x samples). It enables the detection of low-quality samples, drifts, outliers and batch effects in data sets. Visualizations include amongst others bar- and violin plots of the (count/intensity) values, mean vs standard deviation plots, MA plots, empirical cumulative distribution function (ECDF) plots, visualizations of the distances between samples, and multiple types of dimension reduction plots. Furthermore, MatrixQCvis allows for differential expression analysis based on the limma (moderated t-tests) and proDA (Wald tests) packages. MatrixQCvis builds upon the popular Bioconductor SummarizedExperiment S4 class and enables thus the facile integration into existing workflows. The package is especially tailored towards metabolomics and proteomics mass spectrometry data, but also allows to assess the data quality of other data types that can be represented in a SummarizedExperiment object.

Maintained by Thomas Naake. Last updated 5 months ago.

visualizationshinyappsguiqualitycontroldimensionreductionmetabolomicsproteomicstranscriptomics

1.2 match 4.74 score 4 scripts