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Results for “therapeutic games”

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PubMed2026

Game-Based Intervention for Bullying: Assessing the Efficacy of the REThink Therapeutic Game in Primary School Children.

Children's mental health issues can have a lasting effect into adulthood, including enhanced risks for their social and emotional development, as well as their academic performance and overall behavior. Worldwide nearly 1 billion children are affected by the bullying phenomenon, with social, emotional, and economic consequences. In this vein, our study aimed to analyze the effect of the therapeutic game REThink on the improvement of emotion regulation abilities and the reduction of both bullying behavior and victimization in primary school children. Our sample consisted of 75 children who were voluntarily enrolled by their parents, and randomly assigned to the intervention group (n = 38) or to the control group (n = 37). They completed the baseline assessment consisting of emotion regulation, irrationality, bullying and victimization behavior measurements, then the children from the intervention group played the therapeutic game REThink. Four weeks later, after completing each level twice, every participant had completed the same questionnaires at the post-test assessment. The results indicated significant changes across victimization for children who were exposed to verbal, physical or social bullying, increased emotional control and lower levels of irrationality, low frustration tolerance to work and demandingness, with small to medium effect size improvements for the REThink game group compared to the control group. The REThink therapeutic game proved to be a promising intervention tool for reducing victimization effects and irrationality, and improving emotion regulation abilities in primary school children. Future research could improve on these results by addressing the timeline stability limit.

Humans↗

PubMed2026

Stress-driven strategic games in cancer.

Tumor cells face chronic genotoxic, metabolic, hypoxic, and immune stress that shapes their evolution. While stress-response molecular pathways are well characterized, cancer biology lacks a predictive framework for how cells select among alternative adaptive strategies and how these selections interact to produce tumor-level behavior. We propose that evolutionary game theory, previously applied to cooperation in cancer, should be extended to position stress adaptation itself as the organizing principle of tumor evolution. In this framework, stress-adaptive strategies constitute frequency-dependent games whose payoffs depend on population composition. We introduce a three-level distinction between cell states (transcriptional snapshots), game states (local configurations of stress and neighbor composition that define the active payoff structure), and cell strategies (conditional behavioral policies mapping game states to fitness-relevant outputs). This perspective explains the maintenance of intratumor heterogeneity through frequency-dependent selection, the reversibility of resistance through bet-hedging dynamics, and therapy resistance as an equilibrium outcome rather than genetic inevitability. Integrating insights from single-cell genomics, spatial profiling, and lineage tracing, we outline testable predictions and experimental approaches for measuring payoff structures. Therapeutically, the framework suggests exploiting adaptive trade-offs, restricting phenotypic plasticity, and reshaping competitive landscapes. Re-framing cancer as an evolving game of stress adaptation provides a unifying structure for predictive oncology.

Animals↗

PubMed2026

Twisting the End Game: How Telomere Chromatin Modifications Shape Telomere Maintenance.

Cell division inevitably shortens telomeric DNA owing to the end-replication problem. Eukaryotic chromosomes possess specialized telomere structures to maintain genomic stability. In most proliferative cells, telomerase adds telomeric repeats during S-phase. In differentiated cells where telomerase is silenced, telomeres shorten progressively, thereby compromising genomic integrity. Consequently, cancer cells universally activate alternative telomere maintenance mechanisms during malignant transformation: ~80% reactivate telomerase, while a portion of the rest rely on BIR (break-induced replication)-mediated homologous recombination-based ALT (alternative lengthening of telomeres). Although these mechanisms are stable once established, the initial determinants influencing a cancer cell's choice remain poorly understood. This review discusses recent molecular insights into how telomeric chromatin properties profoundly impact this choice. After briefly introducing telomere chromatin characteristics and key players in its maintenance and dynamics, we discuss the mechanisms by which cancer cells acquire distinct telomere replication capabilities. In particular, we present an in-depth analysis linking telomere heterochromatin status to ALT. Furthermore, based on recent advances, we propose a coupled feedforward loop model explaining how the ALT state becomes "locked in" once initiated. Finally, we offer novel perspectives on rational, telomere-centric therapeutic interventions for ALT-positive cancers, focusing on strategies designed to disrupt such feedforward loops by manipulating telomeric chromatin structure.

Humans↗