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Hierarchical Bayesian methods enable information sharing across regression problems on multiple groups of data.

Survival analysis relies fundamentally on the semi-parametric Cox Proportional Hazards (CoxPH) model and the parametric Accelerated Failure Time (AFT) model. CoxPH assumes constant hazard ratios, often failing to capture real-world dynamics, while traditional AFT models are limited by rigid distributional assumptions. Although deep learning models like DeepAFT address these constraints by improving predictive accuracy and handling censoring, they inherit the significant challenge of black-box interpretability. The recent introduction of CoxKAN demonstrated the successful integration of Kolmogorov-Arnold Networks (KANs), a novel architecture that yields highly accurate and interpretable symbolic representations, within the CoxPH framework. Motivated by the interpretability gains of CoxKAN, we introduce KAN-AFT (Kolmogorov Arnold Network-based AFT), the first framework to apply KANs to the AFT model. Our primary contributions include: (i) a principled AFT-KAN formulation, (ii) robust optimization strategies for right-censored observations (e.g., Buckley-James and IPCW), and (iii) an interpretability pipeline that converts the learned spline functions into closed-form symbolic equations for survival time. Empirical results on multiple datasets confirm that KAN-AFT achieves performance comparable to or better than DeepAFT, while uniquely providing transparent, symbolic models of the survival process.

Apart from modeling the time to event, in the presence of competing risks, it is also important to model the event type, or under which risk the event is likely to occur first. Though one can censor subjects with an occurrence of the event under a competing risk other than the risk of special interest, so that every survival model that can handle censoring is able to model competing risks, it is problematic to violate the principle of non-informative censoring [18, 19].

We propose a Bayesian variable selection method in the framework of modal regression for heavy-tailed responses. An efficient expectation-maximization algorithm is employed to expedite parameter estimation. A test statistic is constructed to exploit the shape of the model error distribution to effectively separate informative covariates from unimportant ones. Through simulations, we demonstrate and evaluate the efficacy of the proposed method in identifying important covariates in the presence of non-Gaussian model errors. Finally, we apply the proposed method to analyze two datasets arising in genetic and epigenetic studies.

Hierarchical Bayesian methods enable information sharing across regression problems on multiple groups of data.

We introduce an approach to topic modelling with document-level covariates that remains tractable in the face of large text corpora. This is achieved by de-emphasizing the role of parameter estimation in an underlying probabilistic model, assuming instead that the data come from a fixed but unknown distribution whose statistical functionals are of interest. We propose combining a convex formulation of non-negative matrix factorization with standard regression techniques as a fast-to-compute and useful estimate of such a functional. Uncertainty quantification can then be achieved by reposing non-parametric resampling methods on top of this scheme. This is in contrast to popular topic modelling paradigms, which posit a complex and often hard-to-fit generative model of the data. We argue that the simple, non-parametric approach advocated here is faster, more interpretable, and enjoys better inferential justification than said generative models. Finally, our methods are demonstrated with an application analysing covariate effects on discourse of flavours attributed to Canadian beers.

This paper studies the task of estimating heterogeneous treatment effects in causal panel data models, in the presence of covariate effects. We propose a novel Covariate-Adjusted Deep Causal Learning (CoDEAL) for panel data models, that employs flexible model structures and powerful neural network architectures to cohesively deal with the underlying heterogeneity and nonlinearity of both panel units and covariate effects. The proposed CoDEAL integrates nonlinear covariate effect components (parameterized by a feed-forward neural network) with nonlinear factor structures (modeled by a multi-output autoencoder) to form a heterogeneous causal panel model. The nonlinear covariate component offers a flexible framework for capturing the complex influences of covariates on outcomes. The nonlinear factor analysis enables CoDEAL to effectively capture both cross-sectional and temporal dependencies inherent in the data panel. This latent structural information is subsequently integrated into a customized matrix completion algorithm, thereby facilitating more accurate imputation of missing counterfactual outcomes. Moreover, the use of a multi-output autoencoder explicitly accounts for heterogeneity across units and enhances the model interpretability of the latent factors. We establish theoretical guarantees on the convergence of the estimated counterfactuals, and demonstrate the compelling performance of the proposed method using extensive simulation studies and a real data application.

Predicting cancer dynamics under treatment is challenging due to high inter-patient heterogeneity, lack of predictive biomarkers, and sparse and noisy longitudinal data. Mathematical models can summarize cancer dynamics by a few interpretable parameters per patient. Machine learning methods can then be trained to predict the model parameters from baseline covariates, but do not account for uncertainty in the parameter estimates. Instead, hierarchical Bayesian modeling can model the relationship between baseline covariates to longitudinal measurements via mechanistic parameters while accounting for uncertainty in every part of the model. The mapping from baseline covariates to model parameters can be modeled in several ways. A linear mapping simplifies inference but fails to capture nonlinear covariate effects and scale poorly for interaction modeling when the number of covariates is large. In contrast, Bayesian neural networks can potentially discover interactions between covariates automatically, but at a substantial cost in computational complexity. In this work, we develop a hierarchical Bayesian model of subpopulation dynamics that uses baseline covariate information to predict cancer dynamics under treatment, inspired by cancer dynamics in multiple myeloma (MM), where serum M protein is a well-known proxy of tumor burden. As a working example, we apply the model to a simulated dataset and compare its ability to predict M protein trajectories to a model with linear covariate effects. Our results show that the Bayesian neural network covariate effect model predicts cancer dynamics more accurately than a linear covariate effect model when covariate interactions are present. The framework can also be applied to other types of cancer or other time series prediction problems that can be described with a parametric model.

Statistical approaches that successfully combine multiple datasets are more powerful, efficient, and scientifically informative than separate analyses. To address variation architectures correctly and comprehensively for high-dimensional data across multiple sample sets (i.e., cohorts), we propose multiple augmented reduced rank regression (maRRR), a flexible matrix regression and factorization method to concurrently learn both covariate-driven and auxiliary structured variation. We consider a structured nuclear norm objective that is motivated by random matrix theory, in which the regression or factorization terms may be shared or specific to any number of cohorts. Our framework subsumes several existing methods, such as reduced rank regression and unsupervised multi-matrix factorization approaches, and includes a promising novel approach to regression and factorization of a single dataset (aRRR) as a special case. Simulations demonstrate substantial gains in power from combining multiple datasets, and from parsimoniously accounting for all structured variation. We apply maRRR to gene expression data from multiple cancer types (i.e., pan-cancer) from TCGA, with somatic mutations as covariates. The method performs well with respect to prediction and imputation of held-out data, and provides new insights into mutation-driven and auxiliary variation that is shared or specific to certain cancer types.