Motivation: Most existing methods for predicting causal disease genes rely on specific type of evidence, and are therefore limited in terms of applicability. More often than not, the type of evidence available for diseases varies—for example, we may know linked genes, keywords associated with the disease obtained by mining text, or co-occurrence of disease symptoms in patients. Similarly, the type of evidence available for genes varies—for example, specific microarray probes convey information only for certain sets of genes. In this article, we apply a novel matrix-completion method called Inductive Matrix Completion to the problem of predicting gene-disease associations; it combines multiple types of evidence (features) for diseases and genes to learn latent factors that explain the observed gene–disease associations. We construct features from different biological sources such as microarray expression data and disease-related textual data. A crucial advantage of the method is that it is inductive; it can be applied to diseases not seen at training time, unlike traditional matrix-completion approaches and network-based inference methods that are transductive.Results: Comparison with state-of-the-art methods on diseases from the Online Mendelian Inheritance in Man (OMIM) database shows that the proposed approach is substantially better—it has close to one-in-four chance of recovering a true association in the top 100 predictions, compared to the recently proposed Catapult method (second best) that has <15% chance. We demonstrate that the inductive method is particularly effective for a query disease with no previously known gene associations, and for predicting novel genes, i.e. genes that are previously not linked to diseases. Thus the method is capable of predicting novel genes even for well-characterized diseases. We also validate the novelty of predictions by evaluating the method on recently reported OMIM associations and on associations recently reported in the literature.Availability: Source code and datasets can be downloaded from http://bigdata.ices.utexas.edu/project/gene-disease.Contact: naga86@cs.utexas.edu

We consider the problem of link prediction in signed networks. Such networks arise on the web in a variety of ways when users can implicitly or explicitly tag their relationship with other users as positive or negative. The signed links thus created reflect social attitudes of the users towards each other in terms of friendship or trust. Our first contribution is to show how any quantitative measure of social imbalance in a network can be used to derive a link prediction algorithm. Our framework allows us to reinterpret some existing algorithms as well as derive new ones. Second, we extend the approach of [6], by presenting a supervised machine learning based link prediction method that uses features derived from longer cycles in the network. The supervised method outperforms all previous approaches on 3 networks drawn from sources such as Epinions, Slashdot and Wikipedia. The supervised approach easily scales to these networks, the largest of which has 132k nodes and 841k edges. Most real-world networks have an overwhelmingly large proportion of positive edges and it is therefore easy to get a high overall accuracy at the cost of a high false positive rate. We see that our supervised method not only achieves good accuracy for sign prediction but is also especially effective in lowering the false positive rate.

Correctly identifying associations of genes with diseases has long been a goal in biology. With the emergence of large-scale gene-phenotype association datasets in biology, we can leverage statistical and machine learning methods to help us achieve this goal. In this paper, we present two methods for predicting gene-disease associations based on functional gene associations and gene-phenotype associations in model organisms. The first method, the Katz measure, is motivated from its success in social network link prediction, and is very closely related to some of the recent methods proposed for gene-disease association inference. The second method, called Catapult (Combining dATa Across species using Positive-Unlabeled Learning Techniques), is a supervised machine learning method that uses a biased support vector machine where the features are derived from walks in a heterogeneous gene-trait network. We study the performance of the proposed methods and related state-of-the-art methods using two different evaluation strategies, on two distinct data sets, namely OMIM phenotypes and drug-target interactions. Finally, by measuring the performance of the methods using two different evaluation strategies, we show that even though both methods perform very well, the Katz measure is better at identifying associations between traits and poorly studied genes, whereas Catapult is better suited to correctly identifying gene-trait associations overall.The authors want to thank Jon Laurent and Kris McGary for some of the data used, and Li and Patra for making their code available. Most of Ambuj Tewari's contribution to this work happened while he was a postdoctoral fellow at the University of Texas at Austin.

Suppose we have a sample of instances paired with binary labels corrupted by arbitrary instance-and label-dependent noise. With sufficiently many such samples, can we optimally classify and rank instances with respect to the noise-free distribution? We provide a theoretical analysis of this question, with three main contributions. First, we prove that for instance-dependent noise, any algorithm that is consistent for classification on the noisy distribution is also consistent on the clean distribution. Second, we prove that for a broad class of instance-and label-dependent noise, a similar consistency result holds for the area under the ROC curve. Third, for the latter noise model, when the noise-free class-probability function belongs to the generalised linear model family, we show that the Isotron can efficiently and provably learn from the corrupted sample. arXiv:1605.00751v2 [cs.LG] 4 May 2016Recall the standard generalised linear model (GLM) family of class-probability functions.

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