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Hector Zenil

Publications and source records attributed to Hector Zenil.

At least 19 recordsLinked to original sources

Learning 3D biophysical cell properties from 2D images and cell-population statistics

Inferring 3D cellular properties from 2D microscopy is difficult when a reference instrument reports only population statistics rather than labels for individual cells. Here we develop a population-supervised framework that maps single 2D red-cell images to latent biophysical quantities and aggregates them to mean corpuscular volume, red-cell distribution width and mean corpuscular haemoglobin. The model combines shared local inference, a biophysically structured decoder for volume and haemoglobin, learned instance weighting and device-specific calibration. We formalise conditions under which aggregate observations identify restricted instance predictors, show why population agreement does not by itself identify single-cell properties or 3D geometry, and derive the dispersion penalty induced by subset mean matching. The development dataset comprises 390 specimens and 1,105 acquisitions across six devices, with reported Pearson correlations of 0.86--0.98 against a Sysmex analyser. The framework provides a testable route from 2D images and population supervision to 3D cellular biophysics without claiming explicit 3D reconstruction.

cs.AI

Large Language Models As Shannon Lossy Compressors Not Solomonoff Induction Estimators: The Singularity Is Not Near Without Symbolic Model Synthesis

On the one hand, the question of whether Large Language Models (LLMs) are Solomonoff induction estimators has become an explicit question at the intersection of Algorithmic Information Theory (AIT) and Machine Learning (ML) of great interest. On the other hand, the now old idea of an AI Singularity that requires a reliable positive-feedback process in which a system can generate, evaluate and retain genuine improvements to itself continues to come up and is a recurrent concept in the discussion of AGI. We connect and provide some answers to these issues based on current assumptions and future developments of neurosymbolic ML. We will demonstrate that cross-entropy, negative log-likelihood and cognate next-token objectives do not or cannot, by themselves, implement Solomonoff induction: they optimise fit to a supplied conditional distribution rather than a program-weighted universal mixture. While more compute within a fixed objective can improve fit without changing the inductive principle, additional computational resources do not intrinsically without external hyper-parameter or architectural changes, behave as optimal predictors in the Solomonoff and Levin sense. While the data-processing inequality (DPI) and Levin non-growth remain valid, we will show that for finite learners and finite observers, theoretical boundaries have less relevancy and generate a drift between possible approaches. To this end, we interpret different resource-bounded estimators as finite tools for mechanism search that show divergence, not violation, of (algorithmic) information conservation laws. A neurosymbolic approach is already being taken and adopted by current frontier-model developers, including models like Fable and Astra, embracing aspects of model synthesis through symbolic computation and cannot longer be considered purely statistical LLMs.

cs.IT

Algorithmic Information Dynamics of Learning: A Certified, Differentiable Complexity Controller for Grokking

Algorithmic Information Dynamics (AID) studies systems by perturbing them and measuring changes in algorithmic complexity, but its usual estimator, the Block Decomposition Method, is piecewise constant, restricting the calculus to finite differences. We use $K^{\mathrm{CDM}}_{\mathrm{s}F}$, a certified, differentiable estimator, to bring the calculus into learning dynamics: grokking, where a complexity order parameter is known but has not been made to act. As a transient loss kick, the estimator becomes a controller that accelerates grokking in Levin's description-length--versus-time sense, within a data-dependent Occam boundary whose finite-size trend, $f_c\sim\ln p/p$, is consistent with a coupon-collector interpretation. Ablations show that a complexity gate matches a train-loss gate in rescuing failing seeds with $27\%$ less intervention; among the tested signals, only map complexity marks the transition's completion; the certified prior and the per-parameter $\nabla K$ attribution are both fungible (a uniform-prior sensor makes bit-identical gate decisions, and random supports match $\nabla K$-selected ones above a sparsity threshold); and direct field perturbation shows a nucleation-like response to the Occam field (no linear regime is resolved over the probed amplitudes, so these measurements do not justify a fluctuation--dissipation surrogate), with a finite-field response growing by orders of magnitude toward the phase-transition. These measurements account for the empirically tuned staircase: bang--bang pulses, stall-fired and released on yield, whose iteration plausibly builds the response it exploits. The kick transfers to sparse parity and to a transformer; a sustained weight-space loss fails. The algorithmic estimator's distinct contribution is timing (when to fire and when to release), not attribution.

cs.LG

Enhancing Clinical Decision Support and Differential Diagnosis with Knowledge Graphs, and Retrieval Augmented Generation in Generative AI

Diagnostic error carries a burden, while unconstrained large language models (LLMs) remain vulnerable to hallucination and weak integration of quantitative laboratory dynamics. We developed a decision-support pipeline combining disease-specific biomarker correlation graphs, ordinary differential equations (ODEs), deep sequence classification, and retrieval-augmented generation (RAG). For 103 disease classes from a full blood count (FBC) repository, biomarker networks were used as coupling matrices to generate 30 trajectories per disease (3,090 total). A one-dimensional convolutional neural network (CNN) and long short-term memory (LSTM) network classified disease trajectories and six dynamical clusters. A constrained GPT-4o-mini RAG layer used a 19-pattern BMJ Best Practice/NICE corpus to generate differential diagnoses evaluated for diagnostic suitability, evidential grounding, and clinical plausibility. Across five random-seed runs, disease-level accuracy was $0.940 \pm 0.006$ for the CNN (95\% CI 0.933--0.948) and $0.852 \pm 0.019$ for the LSTM (95\% CI 0.828--0.875); the CNN advantage was 8.87 percentage points (95\% CI 6.47--11.27; $t(4)=10.26$, $p=5.1\times10^{-4}$; Hedges' $g=3.67$). Among 100 sampled RAG cases, 96 parsed successfully; evidence was cited in 97.9\%, the true diagnosis was mentioned in 71.9\%, and the composite score was 3.82/5 with a 47.9\% strict pass rate. The central finding was a decoupling between grounding and diagnostic correctness: classifier-correct versus classifier-wrong outputs differed in diagnostic suitability but not evidential grounding. Post-hoc analysis confirmed a 1.02-point diagnostic-score difference (Mann--Whitney $p=0.0024$; Hedges' $g=0.72$), whereas grounding differed by only $-0.02$ points ($p=0.839$; $g=-0.04$).

q-bio.OT

Measuring in-context algorithmic reasoning in language models against an exact Bayes-optimal reference

Whether large language models perform algorithmic inference or pattern completion is hard to test, because most benchmarks supply answers but no distributional reference for what the shown evidence licenses. F-ICL supplies one exactly: we exhaustively enumerate the 86 million valid programs of length at most 13 on a Turing-complete machine F, complement-symmetrised to remove output-polarity bias, and compute the exact posterior under a declared bounded Levin--Solomonoff prior. It is Bayes-optimal for that stated prior rather than universal, and models are never told it exists, so the score reads the inductive prior their served distribution already encodes. Across 105 serving configurations spanning open models from 0.8B to 675B and frontier systems, models answer up to 92% of queries correctly, yet 45 of the 46 exposing distributions sit farther from the F reference than a keystroke reference. This is not an artefact of task selection: on the bit coordinate, the half the length quota cannot distort, 69 of 80 runs stay below the anchor. Fidelity is inert to scale, which accuracy tracks; continuation improves late without converging; and models un-solve a solved task once per two gains, where the F reference does so once per nine and always repairs it. Because absolute distances are reference-dependent, we prove sequential bounds holding for rival priors: any predictor whose prior gives the reference positive weight has bounded cumulative excess loss, and, in a loss never invoking the reference, any Bayesian mixture giving the realised truth positive mass has a bounded truth-loss budget. On 23,998 trajectories, 86.7% already spend over 10 bits of it. Sequences ending by position nine cannot exclude an arbitrarily large finite constant, so these are lower bounds on what a rival prior must already pay. F-ICL is an open benchmark and toolkit.

cs.LG

Tighter Bounds for Algorithmic Complexity Estimation Using a Reusable Code-Based Block Decomposition Method

The Block Decomposition Method (BDM) was introduced as an alternative to popular lossless compression methods such as LZW for estimating algorithmic complexity from the principles of algorithmic probability and classical information theory. It extends the Coding Theorem Method (CTM) from small objects to larger ones by combining local estimates of algorithmic complexity with a global account of repetition based on Shannon entropy. Here, we introduce a version of BDM in which dependencies between blocks are utilized to reduce the length of the description based on reusable program code in the decomposition of an object, and on conditional descriptions capable of accounting for shared structure between observations. We formalize this allocation of descriptive resources as algorithmic attention. Repeated or related components need not be described independently, and the resulting reduction in description length is governed by the amount of shared algorithmic information. We formulate this extension as a reuse optimization problem, show that exact optimization is NP-hard, derive conditions under which it improves upon independent descriptions, relate the achievable gains to algorithmic mutual information, prove the relationship with the previous BDM version, and provide a roadmap for its implementation using CTM-derived complexity and conditional complexity estimates.

cs.IT

Similarity Analysis of Blood Count Reference Intervals Across Continents Reveals No Reproducible Population or Geography-Linked Structure and Supports Personalised Values

Blood reference intervals (RIs) underpin diagnostic interpretation and therapeutic monitoring worldwide. However, many widely used RI systems originate from limited historical cohorts and have been propagated across health systems without harmonised derivation protocols, shared metadata, or cross-population validation. Consequently, the global RI landscape reflects a heterogeneous mixture of legacy standards and local laboratory practices rather than a biologically grounded framework. Here we examine published Complete Blood Count (CBC) reference intervals, one of the most commonly used laboratory panels worldwide. We compiled CBC RI data from 28 countries and analysed their similarity using variability mapping, hierarchical clustering, information-theoretic distances, cohesion benchmarking, and nonlinear manifold visualisation. Body mass index (BMI) served as a methodological positive benchmark and exhibited clear continent-level clustering (mean cohesion approximately 0.78-0.81). In contrast, CBC reference intervals showed no reproducible geography-linked clustering across methods, with uniformly high cohesion scores (mean approximately 1.27-1.30). Weak signals in red-cell indices (MCV, HGB) were unstable across sexes and distance metrics. This absence of structure should not be interpreted as evidence that current CBC reference intervals represent universal biological standards. Rather, it is more consistent with the fragmented and historically inherited nature of the global RI landscape. These findings indicate that published CBC reference intervals do not encode coherent global structure and provide limited support for universal population-based diagnostic thresholds. Instead, they support a transition toward recalibrated and personalised reference frameworks based on longitudinal individual baselines and harmonised derivation standards.

q-bio.OT

Multi-omic Enriched Blood-Derived Digital Signatures Reveal Mechanistic and Confounding Disease Clusters for Differential Diagnosis

Understanding disease relationships through blood biomarkers offers a pathway toward data-driven taxonomy and precision medicine. In this study, we constructed a digital blood twin, a computational model derived from 103 disease signatures comprising longitudinal hematological and biochemical analytes. Profiles were standardized into a unified disease-analyte matrix, and pairwise Pearson correlations were computed to assess similarity across conditions. Hierarchical clustering revealed consistent grouping of hematopoietic disorders, while metabolic, endocrine, and respiratory diseases were more heterogeneous, reflecting weaker internal cohesion. To evaluate cluster structure, the tree was partitioned at a stringent distance threshold, yielding 16 groups. Enrichment analysis of the largest and most heterogeneous cluster demonstrated convergence on cytokine-signaling pathways, indicating shared inflammatory mechanisms that transcend conventional clinical boundaries. PCA and UMAP corroborated the correlation-based results, consistently separating hematological diseases as a distinct cluster. Random Forest feature selection identified neutrophils, mean corpuscular volume, red blood cell count, and platelet count as the most discriminative analytes, reinforcing the role of hematopoietic markers as key drivers of disease stratification. Collectively, these findings show that blood-derived digital signatures can recover clinically meaningful disease clusters while uncovering mechanistic overlaps across categories. This network physiology framework highlights the potential of integrating routine laboratory data with computational methods to refine disease ontology, map comorbidities, and advance precision diagnostics.

q-bio.OT

Patterns in Individual Blood Count Trajectories in the UK Biobank Characterise Disease-Specific Signatures and Anticipate Pan-Cancer Risk

We investigate the longitudinal behaviour of blood markers from common haematological tests as a marker of disease and as a function of disease progression in a variety of conditions including cancer, cardiovascular disease, and infections. We study confounding and non-confounding factors to allow for the earlier detection of disease and conditions based on their longitudinal signatures from biomarker patterns commonly measured in popular and scalable common blood tests across routine clinical tests, in particular the Complete Blood Count (CBC or FBC). Our analysis with normalised temporal profiles and machine learning techniques even before any symptoms appear demonstrates that analyte-group patterns found in blood testing are disease sensitive and disease specific. We demonstrate that CBC markers contribute to the majority of the predictive signal, while biochemistry and other blood panels provide only a modest additional gain mostly associated to very the individual disease for which the test was designed (e.g. CRP, liver enzymes, blood sugar). Our results demonstrate how regular monitoring, computational intelligence, and machine learning applied to longitudinal CBC data can converge to uncover disease patterns, advancing the potential for precision healthcare and predictive medicine on a mass scale leveraging an existing and pervasive blood test.

q-bio.QM

Integrative Adaptive Indexes from Noisy Routine Haematological Markers can Predict and Discriminate Health Status and Biological Age

For more than two decades, advances in personalised medicine and precision healthcare have largely been based on genomics and other omics data. These strategies aim to tailor interventions to individual patient profiles, promising greater treatment efficacy and more efficient allocation of healthcare resources. Here, we show that widely collected common haematologic markers can reliably predict and discriminate individual chronological age and health status from even noisy sources. Our analysis includes synthetic and real retrospective patient data, including medically relevant and extreme cases, and draws on more than 100\,000 complete blood count records over 13 years from the United States Centers for Disease Control and Prevention's National Health and Nutrition Examination Survey (CDC NHANES). We combine fully explainable risk assessment scores with machine and deep learning techniques to focus on clinically significant patterns and characteristics without functioning purely as a ''black-box model allowing interpretation and control. We validated the results with the UK Biobank, a larger cohort independent of the CDC NHANES and with very different collection techniques, the former a survey and the second a longitudinal study. Unlike current biological ageing indicators, this approach may offer rapid, and scalable implementations of personalised, precision and predictive approaches to healthcare and medicine without or before requiring other specialised, uncommon or costly tests.

q-bio.QM

Can Complexity and Uncomputability Explain Intelligence? SuperARC: A Test for Artificial Super Intelligence Based on Recursive Compression

We introduce an increasing-complexity, open-ended, and human-agnostic metric to evaluate foundational and frontier AI models in the context of Artificial General Intelligence (AGI) and Artificial Super Intelligence (ASI) claims. Unlike other tests that rely on human-centric questions and expected answers, or on pattern-matching methods, the test here introduced is grounded on fundamental mathematical areas of randomness and optimal inference. We argue that human-agnostic metrics based on the universal principles established by Algorithmic Information Theory (AIT) formally framing the concepts of model abstraction and prediction offer a powerful metrological framework. When applied to frontiers models, the leading LLMs outperform most others in multiple tasks, but they do not always do so with their latest model versions, which often regress and appear far from any global maximum or target estimated using the principles of AIT defining a Universal Intelligence (UAI) point and trend in the benchmarking. Conversely, a hybrid neuro-symbolic approach to UAI based on the same principles is shown to outperform frontier specialised prediction models in a simplified but relevant example related to compression-based model abstraction and sequence prediction. Finally, we prove and conclude that predictive power through arbitrary formal theories is directly proportional to compression over the algorithmic space, not the statistical space, and so further AI models' progress can only be achieved in combination with symbolic approaches that LLMs developers are adopting often without acknowledgement or realisation.

cs.AI

Quantum LEGO Learning: A Modular Design Principle for Hybrid Artificial Intelligence

Hybrid quantum-classical learning models increasingly integrate neural networks with variational quantum circuits (VQCs) to exploit complementary inductive biases. However, many existing approaches rely on tightly coupled architectures or task-specific encoders, limiting conceptual clarity, generality, and transferability across learning settings. In this work, we introduce Quantum LEGO Learning, a modular and architecture-agnostic learning framework that treats classical and quantum components as reusable, composable learning blocks with well-defined roles. Within this framework, a pre-trained classical neural network serves as a frozen feature block, while a VQC acts as a trainable adaptive module that operates on structured representations rather than raw inputs. This separation enables efficient learning under constrained quantum resources and provides a principled abstraction for analyzing hybrid models. We develop a block-wise generalization theory that decomposes learning error into approximation and estimation components, explicitly characterizing how the complexity and training status of each block influence overall performance. Our analysis generalizes prior tensor-network-specific results and identifies conditions under which quantum modules provide representational advantages over comparably sized classical heads. Empirically, we validate the framework through systematic block-swap experiments across frozen feature extractors and both quantum and classical adaptive heads. Experiments on quantum dot classification demonstrate stable optimization, reduced sensitivity to qubit count, and robustness to realistic noise.

cs.LG

Systematic Reconstruction of Disease Networks from Longitudinal Blood Data for Causal Discovery and Intervention Analysis

We explore the hyperparameters and introduce a methodological framework to convert disease patterns from time series data of blood test results into correlation graphs for causal hypothesis exploration. The networks represent hypotheses that can then be validated or rejected both for causal discovery and causal analysis (under intervention). We synthetically recreated a repository of 105 typical disease longitudinal patterns extracted from medical guidance and research literature of common blood markers to build a systematic pipeline to translate multidimensional clinical data into intervenable disease networks for causal discovery and causal analysis. This study demonstrates that knowledge graphical models reconstructed from longitudinal data can transform routine medical data into clinically interpretable structures. By integrating multiple thresholding strategies and causal graph design, the framework has the purpose to move beyond statistical correlation toward clinically and testable inference networks. These results highlight a practical pathway for more transparent, explainable, and scalable tools in clinical decision support for AI training, precision healthcare and predictive medicine, offering interpretable, clinically actionable outputs that support safer use of AI in differential diagnosis.

q-bio.OT

XGBoost-Powered Digital Twins Leverage Routine Blood Tests for Early Detection of Cancer and Cardiovascular Disease

Early detection of cancer and cardiovascular diseases is fundamental to improving patient outcomes and reducing healthcare expenditure. Current cancer screening programs are targeted towards specific cancers and are often inaccessible to large parts of the population, particularly in remote regions. This project aimed to develop digital blood twins: machine learning models that leverage routinely collected blood test data, demographics, comorbidities, and prescribed medications, for scalable and cost-effective disease screening. Digital blood twins were constructed using the UK Biobank dataset (n = 373,269). Using age, sex, comorbidities, medication profiles, and blood test z-scores, three iterations of XGBoost classifiers were trained for broad cancer, colorectal cancer, and cardiovascular disease prediction. Model interpretability was achieved through SHAP and dimensionality reduction analyses (UMAP, t-SNE). Broad-category cancer models achieved ROC-AUC = 0.607-0.706. Colorectal cancer prediction demonstrated excellent discrimination (ROC-AUC = 0.816-0.993), and cardiovascular models showed clinical utility, notably for hypertension (ROC-AUC = 0.813, F1 = 0.861). SHAP revealed consistent importance of age, sex, basophil count, and cystatin C. Immune digital blood twins as an agnostic tool demonstrate proof-of-concept feasibility for accessible, low-cost, and scalable screening of cancer and cardiovascular diseases, supporting future integration into predictive and preventive healthcare.

q-bio.OT

Exhaustive Investigation of CBC-Derived Biomarker Ratios for Clinical Outcome Prediction: The RDW-to-MCHC Ratio as a Novel Mortality Predictor in Critical Care

Ratios of common biomarkers and blood analytes are well established for early detection and predictive purposes. Early risk stratification in critical care is often limited by the delayed availability of complex severity scores. Complete blood count (CBC) parameters, available within hours of admission, may enable rapid prognostication. We conducted an exhaustive and systematic evaluation of CBC-derived ratios for mortality prediction to identify robust, accessible, and generalizable biomarkers. We generated all feasible two-parameter CBC ratios with unit checks and plausibility filters on more than 90,000 ICU admissions (MIMIC-IV). Discrimination was assessed via cross-validated and external AUC, calibration via isotonic regression, and clinical utility with decision-curve analysis. Retrospective validation was performed on eICU-CRD (n = 156530) participants. The ratio of Red Cell Distribution Width (RDW) to Mean Corpuscular Hemoglobin Concentration (MCHC), denoted RDW:MCHC, emerged as the top biomarker (AUC = 0.699 discovery; 0.662 validation), outperforming RDW and NLR. It achieved near-universal availability (99.9\% vs.\ 35.0\% for NLR), excellent calibration (Hosmer--Lemeshow $p = 1.0$; $\mathrm{ECE} < 0.001$), and preserved performance across diagnostic groups, with only modest attenuation in respiratory cases. Expressed as a logistic odds ratio, each one standard deviation increase in RDW:MCHC nearly quadrupled 30-day mortality odds (OR = 3.81, 95\% CI [3.70, 3.95]). Decision-curve analysis showed positive net benefit at high-risk triage thresholds. A simple, widely available CBC-derived feature (RDW:MCHC) provides consistent, externally validated signal for early mortality risk. While not a substitute for multivariable scores, it offers a pragmatic adjunct for rapid triage when full scoring is impractical.

q-bio.QM

A Quantitative Approach to Estimating Bias, Favouritism and Distortion in Scientific Journalism

While traditionally not considered part of the scientific method, science communication is increasingly playing a pivotal role in shaping scientific practice. Researchers are now frequently compelled to publicise their findings in response to institutional impact metrics and competitive grant environments. This shift underscores the growing influence of media narratives on both scientific priorities and public perception. In a current trend of personality-driven reporting, we examine patterns in science communication that may indicate biases of different types, towards topics and researchers. We focused and applied our methodology to a corpus of media coverage from three of the most prominent scientific media outlets: Wired, Quanta, and The New Scientist -- spanning the past 5 to 10 years. By mapping linguistic patterns, citation flows, and topical convergence, our objective was to quantify the dimensions and degree of bias that influence the credibility of scientific journalism. In doing so, we seek to illuminate the systemic features that shape science communication today and to interrogate their broader implications for epistemic integrity and public accountability in science. We present our results with anonymised journalist names but conclude that personality-driven media coverage distorts science and the practice of science flattening rather than expanding scientific coverage perception. Keywords : selective sourcing, bias, scientific journalism, Quanta, Wired, New Scientist, fairness, balance, neutrality, standard practices, distortion, personal promotion, communication, media outlets.

cs.DL

Assembly Theory Reduced to Shannon Entropy and Rendered Redundant by Naive Statistical Algorithms

Assembly Theory (AT) and its central measure, the assembly index (Ai), represent an invaluable opportunity to address some of the most persistent and widespread conflations and misconceptions about computability and complexity theory in science. The AT defence embodies several common concurrent misconceptions that pile on each other: the belief that Turing machines impose artefactual constraints, the mischaracterisation of Kolmogorov complexity as inapplicable, and the claims around Ai as different from Shannon entropy or compression algorithms. Here we show that the new arguments advanced by the AT group in their defence, are based on misleading and incomplete experiments that, when completed, show the extent of the correlations and overlapping with popular statistical compression algorithms, conforming with the mathematical equivalence to Shannon entropy previously mathematically proved and reported, which remains undisputed. Through theoretical and empirical analysis, we show that Ai does not offer a path towards fundamental novel causal or informational insights beyond what existing statistical frameworks already offer. Rather than offering a unifying theory of life as the AT authors suggest, we argue that AT obfuscates the field and provides a cautionary example of how the accumulation of conceptual mistakes can lead to a misleading theory. Finally, we show that Ai is a particular limited case of another complexity metric based on algorithmic (Kolmogorov) complexity, consisting of decomposing an object into its causal blocks that goes beyond, and outperforms, AT.

cs.IT

Complexity-Informed Causal Modeling of Neurodevelopmental Trajectories in Pediatric High-Grade Gliomas: Divergences from Neural Stem Cell Signatures

Pediatric high grade gliomas are lethal evolutionary disorders with stalled developmental trajectories and disrupted differentiation hierarchies. We integrate transcriptional and algorithmic network complexity based perturbation analysis to elucidate gene expression patterns and molecular divergence between Diffuse Midline Gliomas and glioblastoma, revealing shared developmental programs steering cell fate decision making. Our complex systems approach supports the emerging paradigm that pediatric high grade gliomas are neurodevelopmental disorders with hybrid lineage identities and disrupted patterning. We identify dysregulated neurodevelopmental and morphogenetic signatures, alongside bioelectric and neurotransmitter signaling programs that alter synaptic organization, neuronal fate commitment, and phenotypic plasticity, regulating glioma phenotypic switching. Causal drivers and regulators of plasticity were predicted as both biomarkers and therapeutic targets, reinforcing the view that pediatric gliomas are disorders of cell fate decisions and collective cellular identity. Decoded plasticity signatures indicate a teleonomic bias toward neural progenitor or neuron like identities, while synaptic transmission gene enrichment supports neuron glioma interactions shaping fate trajectories. These findings advance differentiation therapy as a systems medicine strategy, discovering plasticity regulators to reprogram malignant fates toward stable lineages, offering complex systems based targets for cancer reversion and predictive, preventive, precision oncology.

q-bio.QM