Integrating multimodal datasets in clinical oncology is frequently hindered by high dimensionality and blockwise missingness, where entire data sources are unavailable for specific patient subsets. Standard survival models often struggle with these gaps, leading to biased results or patient exclusion. We introduce Multimodality Stacking with Blockwise missing values (MSB), a late-fusion framework for survival analysis that independently models modality-specific features before aggregating predictions via a cross-validated stacking meta-learner. MSB was validated on the PIONeeR study (n=443 patients, 378 biomarkers across eight heterogeneous sources) to predict progression-free survival in advanced non-small cell lung cancer patients receiving immunotherapy. MSB yielded higher predictive performance (C-index) than baseline algorithms. Improvements varied by baseline strength: linear models showed a 15.9% increase (p<0.001 for the Wilcoxon signed-rank test), random survival forests gained 5.4% (p=0.002), and gradient boosting methods improved by 2.1% (p=0.030). Beyond discrimination, MSB reduced the generalization gap (train-test difference in 5 folds cross-validation repeated 3 times: 0.055 vs 0.380 for linear models). Permutation importance analysis identified routine laboratory markers, clinical features, and PD-L1 expression as primary predictive drivers. Missing block indicators showed negligible importance, suggesting the model learned from biomarker values rather than data availability patterns. MSB provides a statistically validated framework for multimodal survival prediction with blockwise missingness. By enabling systematic biomarker evaluation without requiring complete data, MSB offers a practical tool for predictive modeling in biomedical research, pending external validation. Implementation is available at https://github.com/MohamedBoussena/MSB under Inria license.

A team of scientists from Nanyang Technological University Singapore has developed a new biochip that, when paired with computer vision, can detect quickly and accurately extremely small amounts of microRNAs, which are tiny genetic markers linked to diseases such as heart disease. Published in the scientific journal, the new biosensing platform combines a specially designed nanophotonic chip with AI-automated image analysis. With a tiny drop of blood loaded into the chip, it can rapidly detect multiple microRNA biomarkers. With its integrated AI imaging function, thousands of microRNA signals can be imaged and analysed in a single snapshot. Compared with the current gold standard of detecting microRNA - PCR (polymerase chain reaction) detects tiny amounts of genetic material by copying them many times - the new device can cut detection time from hours to 20 minutes. MicroRNAs are short RNA molecules that help regulate genes that work in the body.

We propose a novel method of understanding disease transformation from a healthy baseline with biomarker-level explainability. By modeling the biomarker covariance matrices of healthy controls and disease states, the perturbation can be individually characterized to accomplish mechanistic explanations of disease trajectories, both at a molecular level and for individual patients. Given a cohort of n patients each measured on p biomarkers, we define the biomarker "Hamiltonian" H = X^T X / n \in R^{p \times p}, where X \in R^{n \times p} is the covariant biomarker matrix. The eigenvectors of H define a set of normal modes of biomarker coordination, and the eigenvalues quantify the energy carried by each mode. In the healthy state, the reference Hamiltonian H_0 governs this structure where disease perturbs H_0 by an additive operator ΔH, thus shifting eigenvalues and rotating eigenvectors in proportion to the severity of pathological disruption. We formalize this framework, derive the spectral change given a disease perturbation, and demonstrate that the projection of a newly diagnosed patient's cumulative biomarker covariance structure onto disease-discriminant eigenmodes constitutes an optimal prognostic statistic for greater precision in disease prognosis. This work serves as a veritable white paper with application across a panoply of disease frameworks from cancer to neurodegenerative disorders.

Clinical diagnosis of the eye is performed over multifarious data modalities including scalar clinical labels, vectorized biomarkers, two-dimensional fundus images, and three-dimensional Optical Coherence Tomography (OCT) scans. Clinical practitioners use all available data modalities for diagnosing and treating eye diseases like Diabetic Retinopathy (DR) or Diabetic Macular Edema (DME). Enabling usage of machine learning algorithms within the ophthalmic medical domain requires research into the relationships and interactions between all relevant data over a treatment period. Existing datasets are limited in that they neither provide data nor consider the explicit relationship modeling between the data modalities. In this paper, we introduce the Ophthalmic Labels for Investigating Visual Eye Semantics (OLIVES) dataset that addresses the above limitation. This is the first OCT and near-IR fundus dataset that includes clinical labels, biomarker labels, disease labels, and time-series patient treatment information from associated clinical trials. The dataset consists of 1268 near-IR fundus images each with at least 49 OCT scans, and 16 biomarkers, along with 4 clinical labels and a disease diagnosis of DR or DME. In total, there are 96 eyes' data averaged over a period of at least two years with each eye treated for an average of 66 weeks and 7 injections. We benchmark the utility of OLIVES dataset for ophthalmic data as well as provide benchmarks and concrete research directions for core and emerging machine learning paradigms within medical image analysis.

"It seems like this past week has been quite challenging for you," a disembodied voice tells me, before proceeding to ask a series of increasingly personal questions. "Have you been feeling down or depressed?" "Can you describe what this feeling has been like for you?" "Does the feeling lift at all when something good happens?" When I respond to each one, my chatbot interviewer thanks me for my honesty and empathises with any issues. By the end of the conversation, I will have also spoken about my sleep patterns, sex drive and appetite for food.

Understanding the dynamic reorganization of brain networks is critical for predicting cognitive decline, neurological progression, and individual variability in clinical outcomes. This work proposes a multimodal graph neural network framework that integrates structural MRI, diffusion tensor imaging, and functional MRI to model spatiotemporal brain network reorganization. Brain regions are represented as nodes and structural and functional connectivity as edges, forming longitudinal brain graphs for each subject. Temporal evolution is captured via fractional stochastic differential operators embedded within graph-based recurrent networks, enabling the modeling of long-term dependencies and stochastic fluctuations in network dynamics. Attention mechanisms fuse multimodal information and generate interpretable biomarkers, including network energy entropy, graph curvature, fractional memory indices, and modality-specific attention scores. These biomarkers are combined into a composite prognostic index to quantify individual risk of network instability or cognitive decline. Experiments on longitudinal neuroimaging datasets demonstrate both predictive accuracy and interpretability. The results highlight the potential of mathematically rigorous, multimodal graph-based approaches for deriving clinically meaningful biomarkers from existing imaging data without requiring new data collection.

Early forecasting of individual cognitive decline in Alzheimer's disease (AD) is central to disease evaluation and management. Despite advances, it is as of yet challenging for existing methodological frameworks to integrate multimodal data for longitudinal personalized forecasting while maintaining interpretability. To address this gap, we present the Neural Koopman Machine (NKM), a new machine learning architecture inspired by dynamical systems and attention mechanisms, designed to forecast multiple cognitive scores simultaneously using multimodal genetic, neuroimaging, proteomic, and demographic data. NKM integrates analytical ($α$) and biological ($β$) knowledge to guide feature grouping and control the hierarchical attention mechanisms to extract relevant patterns. By implementing Fusion Group-Aware Hierarchical Attention within the Koopman operator framework, NKM transforms complex nonlinear trajectories into interpretable linear representations. To demonstrate NKM's efficacy, we applied it to study the Alzheimer's Disease Neuroimaging Initiative (ADNI) dataset. Our results suggest that NKM consistently outperforms both traditional machine learning methods and deep learning models in forecasting trajectories of cognitive decline. Specifically, NKM (1) forecasts changes of multiple cognitive scores simultaneously, (2) quantifies differential biomarker contributions to predicting distinctive cognitive scores, and (3) identifies brain regions most predictive of cognitive deterioration. Together, NKM advances personalized, interpretable forecasting of future cognitive decline in AD using past multimodal data through an explainable, explicit system and reveals potential multimodal biological underpinnings of AD progression.

Patients with rare neurological diseases report cognitive symptoms--"brain fog"--invisible to traditional tests. Proof-of-concept in phenylketonuria (PKU) shows speech-derived "Proficiency in Verbal Discourse" correlates Success would transform episodic neurology into continuous personalized monitoring for millions globally. In phenylketonuria (PKU), adults describe "brain fog" and working memory deficits [ We envision smartphone-based speech analysis integrated with medical databases via RELGT, enabling continuous neurocog-nitive monitoring--transforming reactive episodic care into proactive precision neurology. Parkinson's disease involves hypophonia and speech fluctuations tied to medication Huntington's disease reflects CAG-repeat-driven degrneration and progressive motor-cognitive decline. Wilson's disease presents with dysarthria linked to copper accumulation.