We exploit liver cancer prediction model using machine learning algorithms based on epidemiological data of over 55 thousand peoples from 2014 to the present. The best performance is an AUC of 0.71. We analyzed model parameters to investigate critical risk factors that contribute the most to prediction.
Wildfire is one of the biggest disasters that frequently occurs on the west coast of the United States. Many efforts have been made to understand the causes of the increases in wildfire intensity and frequency in recent years. In this work, we propose static and dynamic prediction models to analyze and assess the areas with high wildfire risks in California by utilizing a multitude of environmental data including population density, Normalized Difference Vegetation Index (NDVI), Palmer Drought Severity Index (PDSI), tree mortality area, tree mortality number, and altitude. Moreover, we focus on a better understanding of the impacts of different factors so as to inform preventive actions. To validate our models and findings, we divide the land of California into 4,242 grids of 0.1 degrees $times$ 0.1 degrees in latitude and longitude, and compute the risk of each grid based on spatial and temporal conditions. To verify the generalizability of our models, we further expand the scope of wildfire risk assessment from California to Washington without any fine tuning. By performing counterfactual analysis, we uncover the effects of several possible methods on reducing the number of high risk wildfires. Taken together, our study has the potential to estimate, monitor, and reduce the risks of wildfires across diverse areas provided that such environment data is available.
Recently, several classifiers that combine primary tumor data, like gene expression data, and secondary data sources, such as protein-protein interaction networks, have been proposed for predicting outcome in breast cancer. In these approaches, new composite features are typically constructed by aggregating the expression levels of several genes. The secondary data sources are employed to guide this aggregation. Although many studies claim that these approaches improve classification performance over single gene classifiers, the gain in performance is difficult to assess. This stems mainly from the fact that different breast cancer data sets and validation procedures are employed to assess the performance. Here we address these issues by employing a large cohort of six breast cancer data sets as benchmark set and by performing an unbiased evaluation of the classification accuracies of the different approaches. Contrary to previous claims, we find that composite feature classifiers do not outperform simple single gene classifiers. We investigate the effect of (1) the number of selected features; (2) the specific gene set from which features are selected; (3) the size of the training set and (4) the heterogeneity of the data set on the performance of composite feature and single gene classifiers. Strikingly, we find that randomization of secondary data sources, which destroys all biological information in these sources, does not result in a deterioration in performance of composite feature classifiers. Finally, we show that when a proper correction for gene set size is performed, the stability of single gene sets is similar to the stability of composite feature sets. Based on these results there is currently no reason to prefer prognostic classifiers based on composite features over single gene classifiers for predicting outcome in breast cancer.
Cancer is a primary cause of human death, but discovering drugs and tailoring cancer therapies are expensive and time-consuming. We seek to facilitate the discovery of new drugs and treatment strategies for cancer using variational autoencoders (VAEs) and multi-layer perceptrons (MLPs) to predict anti-cancer drug responses. Our model takes as input gene expression data of cancer cell lines and anti-cancer drug molecular data and encodes these data with our {sc {GeneVae}} model, which is an ordinary VAE model, and a rectified junction tree variational autoencoder ({sc JTVae}) model, respectively. A multi-layer perceptron processes these encoded features to produce a final prediction. Our tests show our system attains a high average coefficient of determination ($R^{2} = 0.83$) in predicting drug responses for breast cancer cell lines and an average $R^{2} = 0.845$ for pan-cancer cell lines. Additionally, we show that our model can generates effective drug compounds not previously used for specific cancer cell lines.
The use of machine learning systems to support decision making in healthcare raises questions as to what extent these systems may introduce or exacerbate disparities in care for historically underrepresented and mistreated groups, due to biases implicitly embedded in observational data in electronic health records. To address this problem in the context of clinical risk prediction models, we develop an augmented counterfactual fairness criteria to extend the group fairness criteria of equalized odds to an individual level. We do so by requiring that the same prediction be made for a patient, and a counterfactual patient resulting from changing a sensitive attribute, if the factual and counterfactual outcomes do not differ. We investigate the extent to which the augmented counterfactual fairness criteria may be applied to develop fair models for prolonged inpatient length of stay and mortality with observational electronic health records data. As the fairness criteria is ill-defined without knowledge of the data generating process, we use a variational autoencoder to perform counterfactual inference in the context of an assumed causal graph. While our technique provides a means to trade off maintenance of fairness with reduction in predictive performance in the context of a learned generative model, further work is needed to assess the generality of this approach.