Non-Crossing Deep Quantile Regression for Distributional Survival Prediction

In survival analysis the way covariates act on the risk of an event often differs between early and late failure times, yet hazard- and mean-based summaries collapse this variation into a single number. Quantile-based modeling instead describes the full conditional distribution on the original time scale, but existing censored-data methods are either inflexible or produce logically inconsistent crossing quantile curves. We propose a Censored Non-crossing Quantile (CNQ) framework for right-censored data that jointly estimates several conditional survival quantiles and guarantees valid ordering by construction, with flexibility supplied by Kolmogorov-Arnold and Transformer backbones, and we establish a finite-sample excess-risk bound holding jointly across all fitted quantile levels. Across 27 simulation settings and six cohorts the framework attains lower pinball loss than quantile-, hazard- and tree-based competitors whenever the conditional distribution is asymmetric, with interval coverage closer to nominal on all six. In two clinical case studies (METABRIC, breast cancer; FLCHAIN, population mortality) it recovers covariate effects that vary across the survival distribution and would be hidden by a single hazard ratio, and yields coherent individualized quantile milestones. Code: https://github.com/BIG-S2/deepcnq

Separating Spatial and Clinical Risk with Node-Splitting SVM Survival Trees

Recovering geographic variation in survival requires separating spatial risk from patients' clinical characteristics, a problem complicated by prognostic covariates that are themselves spatially structured. We develop a nonparametric two-stage method for this separation. A clinical survival tree fit to the covariates alone supplies leaf Nelson-Aalen cumulative hazard residuals, transferring the censored survival structure to a clinically adjusted scale without imposing a functional form on the clinical hazard, and a second tree fit to these residuals on the coordinates recovers the spatial structure. Both stages are kernel dipole-splitting survival trees, so the resulting spatial risk map is piecewise constant, with sharp, possibly curved boundaries. We establish when the residuals recover the spatial signal: under a multiplicative frailty and an exogeneity condition, they are free of the clinical covariates given location and stochastically ordered by the frailty. An expansion of the frailty Laplace exponent quantifies their approximate exponentiality and identifies the leading remainder. These results assume consistency of the first stage rather than a model class, so the construction extends to other survival estimators. On the LeukSurv leukemia data the method agrees with a Bayesian Gaussian random field frailty about where risk is elevated while resolving sharp adjacencies the smooth surface averages away, and an unadjusted spatial analysis misattributes clinical variation to location. Simulations with known zones, including a sweep through graded violations of exogeneity, locate the point at which the two contributions cease to be separately identifiable, with the smooth benchmark degrading in parallel as that point is approached.

Surv-IPTB: An Attention-Based Model for Estimating Individual Probability of Treatment Benefit with Survival Data

This work presents a novel attention-based framework for estimating the Individual Probability of Treatment Benefit (IPTB) in survival analysis contexts. The proposed model, called Surv-IPTB, directly quantifies the probability that a specific patient will experience extended survival time under treatment versus control. We reformulate IPTB estimation as a binary classification problem, leveraging pairwise patient comparisons across treatment and control cohorts. The framework incorporates a principled handling of right-censored observations through imprecise probability representations, where uncertain treatment effects are characterized by interval-valued probabilities. An attention mechanism with learnable query-key transformations enables flexible, data-driven aggregation of pairwise comparisons, while simultaneously learning soft class probabilities for censored cases. Through extensive experiments on synthetic datasets with complex nonlinear structures, including spiral, bell-shaped, and circular feature spaces, we demonstrate that our approach maintains robust performance across varying censoring rates and treatment effect strengths. The model consistently outperforms meta-learner baselines (T-learner and S-learner) equipped with random survival forests, Cox proportional hazards, and Beran estimators, particularly in challenging nonlinear scenarios where conventional methods exhibit significant degradation. The results establish the proposed attention-based framework as a scalable and statistically principled solution for personalized treatment benefit assessment in survival settings. The code implementing the model is publicly available.

Seeing Below the Limit of Detection: A Censored-Poisson Bayesian Latent-Growth Change-Point Detector (the Span Detector) for Serial ctDNA in HR+/HER2- Metastatic Breast Cancer

Circulating-tumour DNA (ctDNA) carries evidence of drug resistance months before imaging shows it, but the earliest evidence lives below the assay's limit of detection (LoD): a nascent subclone is detected only intermittently, producing a flickering sequence of faint detects and non-detects. Commercial liquid biopsies treat each draw as an independent snapshot and a non-detect as nothing. We argue a non-detect is a left-censored observation, and the pattern of non-detects and faint detects over time carries actionable evidence of growth before any single value is trustworthy. We introduce Span, a censored-Poisson Bayesian latent-growth change-point detector that models the binary detection process, accumulates a sequential generalised-likelihood-ratio statistic for an upward change-point in the per-variant detection rate, and raises a competing-risks alarm with calibrated false-alarm control. Span has no learned weights, so there is nothing to overfit. On a synthetic cohort of HR+/HER2- metastatic breast cancer on first-line CDK4/6-inhibitor plus endocrine therapy, at a matched 10% false-alarm rate, Span roughly doubles the fraction of impending progressions caught three months ahead (indolent regime: 25% vs 11% for the snapshot), with a falsifiable dose-response: large for indolent emergence, vanishing for fast emergence. A value-trajectory baseline performs identically to the snapshot, isolating the gain to the censored detection model. The survival backbone matches a Cox baseline on real breast-cancer data (GBSG-2, n=686; C-index 0.67 vs 0.68), and on a real longitudinal cohort with clean biomarkers (PBC2, n=312) the same pipeline correctly declines to win, a falsifiable boundary test confirming the mechanism is regime-specific. All ctDNA trajectories are synthetic.

SurvPFN: Towards Foundation Models for Survival Predictions

Tabular foundation models (TFMs) have made rapid progress in standard classification and regression, but time-to-event survival prediction tasks have remained largely untouched. Unlike in standard regression tasks, survival prediction models must account for censored data. Standard TFMs cannot handle natively censored data, leading to biased and inaccurate predictions, making them unsuitable for real-world applications. To overcome this fundamental limitation, we propose \texttt{SurvPFN}, a prior-data fitted network (PFN), for survival prediction tasks. We pretrain \texttt{SurvPFN} on millions of synthetic survival prediction tasks to learn survival via distributional regression that accounts for censored data. \texttt{SurvPFN} works by (1) generating data with Weibull event times and a non-informative censoring mechanism; (2) integrating a censored event indicator; and (3) minimizing a censored negative log-likelihood. On SurvSet, a collection of real-world survival tasks, \texttt{SurvPFN} is highly competitive with classical and deep survival baselines without per-dataset fitting, a survival-specific architecture, or feature engineering. We show that survival can be treated as a continuous-time distributional regression problem with censored loss, unlocking the power of PFNs for time-to-event predictions.

SDPM: Survival Diffusion Probabilistic Model for Continuous-Time Survival Analysis

Survival analysis aims to estimate a time-to-event distribution from data with censored observations. Many existing methods either impose structural assumptions on the hazard function or discretize the time axis, which may limit flexibility and introduce approximation errors. We propose the Survival Diffusion Probabilistic Model (SDPM), a generative approach to continuous-time survival analysis. SDPM models the conditional distribution of the survival outcome, represented by the pair of observed time and censoring indicator, $\mathbb{P}(T,δ\mid \mathbf{x})$, using a denoising diffusion model. Under the assumption of conditionally independent censoring, conditional samples generated by the model can be transformed into survival function estimates using the Kaplan-Meier estimator. This formulation avoids parametric assumptions on the event-time distribution and does not require a discretization of the output time space. The model operates in a transformed target space, using standardized log-times and a continuous Gaussian-mixture representation of the censoring indicator. We evaluate SDPM on ten real survival datasets and compare it with five strong baselines, including tree-based, boosting-based, and neural survival models. Results show that SDPM achieves competitive predictive performance across C-index, integrated time-dependent AUC, and integrated Brier score. A study on synthetic Cox-Weibull data demonstrates that SDPM can recover the shape of an underlying continuous survival distribution more accurately than a strong nonparametric baseline when sufficiently many samples are generated. An ablation study confirms the importance of the proposed target-space transformations, which improve event-rate calibration, reduce invalid generated times, and provide consistent gains in predictive discrimination. Codes implementing the proposed model are publicly available.