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Biology subjects

Li, Q.

Publications and source records attributed to Li, Q..

At least 415 records · Page 23Linked to original sources

Self-assembly vascularized human cardiac organoids model cardiac diseases in petri dishes and in mice

In this study, we generated self-assembly cardiac organoids (COs) from human pluripotent stem cells by dual-phase modulation of Wnt/{beta}-catenin pathway, utilizing CHIR99021 and IWR-1-endo. The resulting COs exhibited a diverse array of cardiac-specific cell lineages, cardiac cavity-like structures and demonstrated the capacity of spontaneous beating and vascularization in vitro. We further employed these complex and functional COs to replicate conditions akin to human myocardial infarction and SARS-CoV-2 induced fibrosis. These models accurately captured the pathological characteristics of these diseases, in both in vitro and in vivo settings. In addition, we transplanted the COs into NOD SCID mice and observed that they survived and exhibited ongoing expansion in vivo. Impressively, over a span of 75-day transplantation, these COs not only established blood vessel-like structures but also integrated with the host mices vascular system. It is noteworthy that these COs developed to a size of approximately 8 mm in diameter, slightly surpassing the dimensions of the mouse heart. This innovative research highlighted the potential of our COs as a promising avenue for cardiovascular research and therapeutic exploration.

cell biology↗

Long-term breast cancer response to CDK4/6 inhibition defined by TP53-mediated geroconversion

Inhibition of CDK4/6 kinases has led to improved outcomes in breast cancer. Nevertheless, only a minority of patients experience long-term disease control. Using a clinically-annotated cohort of patients with metastatic HR+ breast cancer, we identified TP53 loss (28.8%) and MDM2 amplification (6.7%) to be associated with lack of long-term disease control. Human breast cancer models revealed that p53 loss did not affect CDK4/6 activity or G1-blockade, but instead promoted drug-insensitive p130 phosphorylation by CDK2. Persistence of phospho-p130 prevented DREAM complex assembly, enabling cell cycle reentry and tumor progression. Inhibitors of CDK2 could overcome p53 loss, leading to geroconversion and manifestation of senescence phenotypes. Complete inhibition of both CDK4/6 and CDK2 kinases appears to be necessary to facilitate long-term response across genomically-diverse HR+ breast cancers.

cancer biology↗

Predictive evolutionary modelling for influenza virus by site-based dynamics of mutations

A predictive evolutionary model was developed to forecast representative influenza viral strains and select vaccine strains for upcoming epidemic seasons. Influenza virus continuously evolves to escape human adaptive immunity and generates seasonal epidemics. A computational approach beth-1 that models site-wise mutation dynamics demonstrated remarkable matching of predicted strains to the circulating viruses in subsequent seasons for the influenza A(H1N1)pdm09 and A(H3N2) viruses in both retrospective and prospective validations. The method offers a promising and ready-to-use tool to facilitate vaccine strain selection for the influenza virus, achieved by capturing heterogeneous evolutionary dynamics over genome space-time and linking molecular variants to population immune response. One-Sentence SummaryA computational model predicts virus evolution and facilitates vaccine strain selection for the influenza virus

evolutionary biology↗

Revealing Complex Functional Topology Brain Network Correspondences Between Humans and Marmosets

Functional correspondences are known to exist within the brains of both human and non-human primates; however, our understanding of this phenomenon remains largely incomplete. The examination of the topological characteristics inherent in whole-brain functional connectivity bears immense promise in elucidating shared as well as distinctive patterns across different species. In this investigation, we applied topological graph analysis to brain networks and scrutinized the congruencies and disparities within the connectomes of human and marmoset monkey brains. The findings brought to light noteworthy similarities in functional connectivity patterns distributed across the entire brain, with a particular emphasis on the dorsal attention network, default mode network and visual network. Moreover, we discerned unique neural connections between humans and marmosets during both resting and task-oriented states. In essence, our study reveals a combination of shared and divergent functional brain connections underlying spontaneous and specific cognitive functions across these two species.

biophysics↗

weIMPUTE: A User-Friendly Web-Based Genotype Imputation Platform

Genotype imputation is a critical preprocessing step in genome-wide association studies (GWAS), enhancing statistical power for detecting associated single nucleotide polymorphisms (SNPs) by increasing marker size. In response to the needs of researchers seeking user-friendly graphical tools for imputation without requiring informatics or computer expertise, we have developed weIMPUTE, a web-based imputation graphical user interface (GUI). Unlike existing genotype imputation software, weIMPUTE supports multiple imputation software, including SHAPEIT, Eagle, Minimac4, Beagle, and IMPUTE2, while encompassing the entire workflow, from quality control to data format conversion. This comprehensive platform enables both novices and experienced users to readily perform imputation tasks. For reference genotype data owners, weIMPUTE can be installed on a server or workstation, facilitating web-based imputation services without data sharing. weIMPUTE represents a versatile imputation solution for researchers across various fields, offering the flexibility to create personalized imputation servers on different operating systems.

bioinformatics↗

Development of connectome dynamics at birth predicts neurocognitive outcomes at age 2

The functional connectome of the human brain comprises time-varying network structure that facilitates efficient inter-module communication and support flexible cognitive functions. However, little is known about how the connectome dynamics of the brain emerges and develops at very early stages of human life and whether this dynamics is predictive of neurocognitive outcomes later in life. Here, we employed resting-state functional MRI data from 39 infants (31 to 42 postmenstrual weeks) and a multilayer network model to characterize the development of connectome dynamics during the third trimester and its critical role in predicting future neurocognitive outcomes at 2 years of age. We observed that the modular architecture of baby functional connectomes spontaneously reconfigures over time, with lower network module switching across time primarily in the primary regions and higher module switching mainly in the association areas. With development, the dynamic switching between the brain modules was significantly decreased, primarily located in the lateral precentral gyrus, medial temporal lobe, and subcortical areas. The clustering analysis further revealed that the primary areas displayed a higher developmental rate than the higher-order systems. Using the support vector regression approach, we found that brain connectome dynamics at birth significantly predicted cognitive and language performance at 2 years of age. Our findings highlight the emergence and spatially inhomogeneous maturation of the neonate connectome dynamics, laying a critical neural foundation for the development of cognitive and language skills later in life.

neuroscience↗

Chrombus-XMBD: A Graph Generative Model Predicting 3D-Genome, ab initio from Chromatin Features

AbstractsThe landscape of 3D-genome is crucial for transcription regulation. But capturing the dynamics of chromatin conformation is costly and technically challenging. Here we described "Chrombus-XMBD", a graph generative model capable of predicting chromatin interactions ab inito based on available chromatin features. Chrombus employes dynamic edge convolution with QKV attention setup, which maps the relevant chromatin features to a learnable embedding space thereby generate genomewide 3D-contactmap. We validated Chrombus predictions with published databases of topological associated domains (TAD), eQTLs and gene-enhancer interactions. Chrombus outperforms existing algorithms in efficiently predicting long-range chromatin interactions. Chrombus also exhibits strong generalizability across different cell lineage and species. Additionally, the parameter sets of Chrombus inform the biological processes underlying 3D-genome. Our model provides a new perspective towards interpretable AI-modeling of the dynamics of chromatin interactions and better understanding of cis-regulation of gene expression.

bioinformatics↗

Rapid and visual detection of Schistosoma japonicum circulating nucleic acids by CRISPR-Cas12a

BackgroundSchistosomiasis is the second most destructive parasitic disease globally. It poses a serious threat to human health if not diagnosed and treated promptly. However, the current detection methods have limitations due to their dependence on specialized equipments and personnel, and the long detection time, resulting in less-than-ideal detection outcomes. Therefore, more accurate and sensitive assays are required to aid in the control of schistosomiasis. This study aims to develop a rapid and practical method for detecting Schistosoma japonicum circulating nucleic acid by combining the Cas12a protein in the CRISPR (Clustered regularly interspaced short palindromic repeats) system with recombinase-mediated isothermal nucleic acid amplification technology. Methodology/Principal FindingsWe created a CRISPR-Cas12a detection method for Schistosomiasis. SjR2 and SjCHGCS19 genes with repetitive copies in the Schistosoma japonicum genome were targeted for detection. The CRISPR-Cas12a detection method can achieve a detection sensitivity of 1 cp/{micro}L, with no cross-reaction with the other three human-infecting trematode parasites. To vividly simulate clinical patients at different infection stages, we collected rabbits serums at 1 d, 3 d, 1 w, 3 w, 5 w, and 7 w post-infection. Circulating Schistosoma japonicum DNA in the serum can be detected as early as 3 days post-infection. The sample and positive rates of each stage were analyzed and the CRISPR-Cas12a detection method prevailed to Nested-PCR. Additionally, our assay offers flexible results readout options, including lateral test strips. Conclusions/SignificanceThis CRISPR-Cas12a detection method enables sensitive and specific detection of Schistosomiasis by detecting highly repetitive SjR2 and SjCHGCS19 genes. The method was fully validated with rabbits serums collected at different infection stages, which can be applied to monitoring the early infection of schistosomiasis in resource-limited regions. Author SummaryWith the development of schistosomiasis prevention and control efforts in recent years, the prevalence rate and infection intensity of schistosomiasis have decreased, making early and accurate diagnoses more challenging. Combining CRISPR-Cas12a protein with isothermal amplification technology, a detection method for the multi-copy sequences SjR2 and SjCHGCS19 in the genome of Schistosoma japonicum was developed in this study. The results demonstrated that the detection sensitivity of this method could reach 1 cp/{micro}L, with no cross reactivity with three other fluke-like human parasites. In this study, serum samples from 15 rabbits infected with Schistosoma japonicum were used to validate the method. The results demonstrated that rabbits could be identified as early as the third day after infection. CRISPR-Cas12a detection method has a higher positive rate than traditional Nested-PCR. In addition, lateral test strips enable direct observation of our assay results. The aforementioned research findings indicate that the CRISPR-Cas12a-based detection method can be utilized for the early diagnosis of schistosomiasis. In conjunction with the result reading method of the lateral test strips, it also provides a new method for the on-site diagnosis of schistosomiasis in environments with limited access to resources.

bioengineering↗

Altered Fhod3 Expression Involved in Progressive High-Frequency Hearing Loss via Dysregulation of Actin Polymerization Stoichiometry in The Cuticular Plate

Age-related hearing loss (ARHL) is a common sensory impairment with complex underlying mechanisms. In our previous study, we performed a meta-analysis of genome-wide association studies (GWAS) in mice and identified a novel locus on chromosome 18 associated with ARHL specifically linked to a 32 kHz tone burst stimulus. Consequently, we investigated the role of Formin Homology 2 Domain Containing 3 (Fhod3), a newly discovered candidate gene for ARHL based on the GWAS results. We observed Fhod3 expression in auditory hair cells (HCs) and primarily localized at the cuticular plate (CP). To understand the functional implications of Fhod3 in the cochlea, we generated Fhod3 overexpression mice (Pax2-Cre+/-; Fhod3Tg/+) (TG) and HC-specific conditional knockout mice (Atoh1-Cre+/-; Fhod3fl/fl) (KO). Audiological assessments in TG mice demonstrated progressive high-frequency hearing loss, characterized by predominant loss of outer hair cells, and a decreased phalloidin intensities of CP. Ultrastructural analysis revealed shortened stereocilia in the basal turn cochlea. Importantly, the hearing and HC phenotype in TG mice were replicated in KO mice. These findings indicate that Fhod3 plays a critical role in regulating actin dynamics in CP and stereocilia. Further investigation of Fhod3 related hearing impairment mechanisms may facilitate the development of therapeutic strategies for ARHL in humans.

neuroscience↗

Autoencoder-transformed transcriptome improves genotype-phenotype association studies

Transcriptome-wide association study (TWAS) is an emerging model leveraging gene expressions to direct genotype-phenotype association mapping. A key component in TWAS is the prediction of gene expressions; and many statistical approaches have been developed along this line. However, a problem is that many genes have low expression heritability, limiting the performance of any predictive model. In this work, hypothesizing that appropriate denoising may improve the quality of expression data (including heritability), we propose AE-TWAS, which adds a transformation step before conducting standard TWAS. The transformation is composed of two steps by first splitting the whole transcriptome into co-expression networks (modules) and then using autoencoder (AE) to reconstruct the transcriptome data within each module. This transformation removes noise (including nonlinear ones) from the transcriptome data, paving the path for downstream TWAS. We showed two inspiring properties of AE-TWAS: (1) After transformation, the transcriptome data enjoy higher expression heritability at the low-heritability spectrum and possess higher connectivity within the modules. (2) The transferred transcriptome indeed enables better performance of TWAS; and moreover, the newly formed highly connected genes (i.e., hub genes) are more functionally relevant to diseases, evidenced by their functional annotations and overlap with TWAS hits.

bioinformatics↗

ScopeViewer: A Browser-Based Solution for Visualizing Spatial Transcriptomics Data

MotivationSpatial transcriptomics (ST) enables a high-resolution interrogation of molecular characteristics within specific spatial contexts and tissue morphology. Despite its potential, visualization of ST data is a challenging task due to the complexities in handling, sharing and visualizing large image datasets together with molecular information. ResultsWe introduce ScopeViewer, a browser-based software designed to overcome these challenges. ScopeViewer offers the following functionalities: (1) It visualizes large image data and associated annotations at various zoom levels, allowing for intricate exploration of the data; (2) It enables dual interactive viewing of the original images along with their annotations, providing a comprehensive understanding of the context; (3) It displays spatial molecular features with optimized bandwidth, ensuring a smooth user experience; and (4) It bolsters data security by circumventing data transfers. AvailabilityScopeViewer is available at: https://datacommons.swmed.edu/scopeviewer ContactXiaowei.Zhan@UTSouthwestern.edu, Guanghua.Xiao@UTSouthwestern.edu Supplementary informationSupplementary data are available at Bioinformatics online.

bioinformatics↗

AMPK targets PDZD8 to trigger carbon source shift to glutamine

The shift of carbon utilisation from glucose to other nutrients is a fundamental metabolic adaptation to cope with the decreased glucose oxidation during fasting or starvation1. AMP-activated protein kinase (AMPK) plays crucial roles in manifesting physiological benefits accompanying glucose starvation or calorie restriction2. However, the underlying mechanisms are unclear. Here, we show that low glucose-induced activation of AMPK plays a decisive role in the shift of carbon utilisation from glucose to glutamine. We demonstrate that endoplasmic reticulum (ER)-localised PDZD8, which we identify to be a new substrate of AMPK, is required for the glucose starvation-promoted glutaminolysis. AMPK phosphorylates PDZD8 at threonine 527 (T527), and promotes it to interact with and activate the mitochondrial glutaminase 1 (GLS1), a rate-limiting enzyme of glutaminolysis3-5, and as a result the ER-mitochondria contact is strengthened. In vivo, PDZD8 enhances glutaminolysis, and triggers mitohormesis that is required for extension of lifespan and healthspan in Caenorhabditis elegans subjected to glucose starvation or caloric restriction. Muscle-specific re-introduction of wildtype PDZD8, but not the AMPK-unphosphorylable PDZD8-T527A mutant, to PDZD8-/- mice is able to rescue the increase of glutaminolysis, and the rejuvenating effects of caloric restriction in aged mice, including grip strength and running capacity. Together, these findings reveal an AMPK-PDZD8-GLS1 axis that promotes glutaminolysis and executes the anti-ageing effects of calorie restriction by promoting inter-organelle crosstalk between ER and mitochondria.

cell biology↗

rvTWAS: identifying gene-trait association using sequences by utilizing transcriptome-directed feature selection

Towards the identification of genetic basis of complex traits, transcriptome-wide association study (TWAS) is successful in integrating transcriptome data. However, TWAS is only applicable for common variants, excluding rare variants in exome or whole genome sequences. This is partly because of the inherent limitation of TWAS protocols that rely on predicting gene expressions. Briefly, a typical TWAS protocol has two steps: it trains an expression prediction model in a reference dataset containing gene expressions and genotype, and then applies this prediction model to a genotype-phenotype dataset to "impute" the unobserved expression (that is called GReX) to be associated to the phenotype. In this procedure, rare variants are not used due to its low power in predicting expressions. Our previous research has revealed the insight into TWAS: the two steps are essentially genetic feature selection and aggregations that do not have to involve predictions. Based on this insight disentangling TWAS, rare variants inability of predicting expression traits is no longer an obstacle. Herein, we developed "rare variant TWAS", or rvTWAS, that first uses a Bayesian model to conduct expression-directed feature selection and then use a kernel machine to carry out feature aggregation, forming a model leveraging expressions for association mapping including rare variants. We demonstrated the performance of rvTWAS by thorough simulations and real data analysis in three psychiatric disorders, namely schizophrenia, bipolar disorder, and autism spectrum disorder. rvTWAS will open a door for sequence-based association mappings integrating gene expressions.

bioinformatics↗

XA4C: eXplainable representation learning via Autoencoders revealing Critical genes

Machine Learning models have been frequently used in transcriptome analyses. Particularly, Representation Learning (RL), e.g., autoencoders, are effective in learning critical representations in noisy data. However, learned representations, e.g., the "latent variables" in an autoencoder, are difficult to interpret, not to mention prioritizing essential genes for functional follow-up. In contrast, in traditional analyses, one may identify important genes such as Differentially Expressed (DiffEx), Differentially Co-Expressed (DiffCoEx), and Hub genes. Intuitively, the complex gene-gene interactions may be beyond the capture of marginal effects (DiffEx) or correlations (DiffCoEx and Hub), indicating the need of powerful RL models. However, the lack of interpretability and individual target genes is an obstacle for RLs broad use in practice. To facilitate interpretable analysis and gene-identification using RL, we propose "Critical genes", defined as genes that contribute highly to learned representations (e.g., latent variables in an autoencoder). As a proof-of-concept, supported by eXplainable Artificial Intelligence (XAI), we implemented eXplainable Autoencoder for Critical genes (XA4C) that quantifies each genes contribution to latent variables, based on which Critical genes are prioritized. Applying XA4C to gene expression data in six cancers showed that Critical genes capture essential pathways underlying cancers. Remarkably, Critical genes has little overlap with Hub or DiffEx genes, however, has a higher enrichment in a comprehensive disease gene database (DisGeNET), evidencing its potential to disclose massive unknown biology. As an example, we discovered five Critical genes sitting in the center of Lysine degradation (hsa00310) pathway, displaying distinct interaction patterns in tumor and normal tissues. In conclusion, XA4C facilitates explainable analysis using RL and Critical genes discovered by explainable RL empowers the study of complex interactions. Author SummaryWe propose a gene expression data analysis tool, XA4C, which builds an eXplainable Autoencoder to reveal Critical genes. XA4C disentangles the black box of the neural network of an autoencoder by providing each genes contribution to the latent variables in the autoencoder. Next, a genes ability to contribute to the latent variables is used to define the importance of this gene, based on which XA4C prioritizes "Critical genes". Notably, we discovered that Critical genes enjoy two properties: (1) Their overlap with traditional differentially expressed genes and hub genes are poor, suggesting that they indeed brought novel insights into transcriptome data that cannot be captured by traditional analysis. (2) The enrichment of Critical genes in a comprehensive disease gene database (DisGeNET) is higher than differentially expressed or hub genes, evidencing their strong relevance to disease pathology. Therefore, we conclude that XA4C can reveal an additional landscape of gene expression data.

bioinformatics↗

Host-microbiota interactions contributing to the heterogeneous tumor microenvironment in colorectal cancer

BackgroundColorectal cancer (CRC) is a highly heterogeneous cancer with four consensus molecular subtypes (CMSs) characterized by distinct tumor microenvironment (TME). We aimed to depict the characteristics of host-microbiota interactions and their contributions to TME in each CMS. MethodsHost transcriptome and intratumoral microbiome profiles of 594 CRC samples were derived from RNA-Seq data from TCGA. Differential host genes and microbes among CMSs were identified. Immune microenvironments were assessed by CIBERSORTx and ESTIMATE and microbial co-abundance analyses were performed by FastSpar. Host-microbiota associations were evaluated by LASSO penalized regression in each CMS. ResultsAlong with distinct host gene signatures, including ferroptosis-related genes and immune microenvironments, 293, 153, 66 and 109 intratumoral differential microbial genera were identified within each of the four CMSs, respectively. Furthermore, the host-microbiota interactions contributed to distinct TME in each CMS, represented by 829, 1,270, 634 and 1,882 robust gene-microbe associations, respectively. The TME in CMS1 was featured with inflammation-related HSF1 activation and interactions between genes of endothelin pathway and Flammeovirga. Integrins-related genes positively correlated with Sutterella in CMS2 while CMS3 displayed microbial associations with biosynthetic and metabolic pathways. Genes in collagens biosynthesis positively correlated with Sutterella, contributing to homeostasis disturbance in CMS4. Besides, ferroptosis dysregulation was more remarkable in immune-high subtypes, which might partly result from the colonization of tissue microbes. ConclusionsWe systematically profiled the landscapes of TME, of each CMS in CRC, encompassing host genes, intratumoral microbiome and their interactions, which could illuminate novel mechanisms for the heterogeneity in CRC and potential therapeutic targets.

microbiology↗

An expression-directed linear mixed model (edLMM) discovering low-effect genetic variants

Detecting genetic variants with low effect sizes using a moderate sample size is difficult, hindering downstream efforts to learn pathology and estimating heritability. In this work, by utilizing informative weights learned from training genetically predicted gene expression models, we formed an alternative approach to estimate the polygenic term in a linear mixed model (LMM). Our LMM estimates the genetic background by incorporating their relevance to gene expression. Our protocol, expression-directed linear mixed model (edLMM), enables the discovery of subtle signals of low-effect variants using moderate sample size. By applying edLMM to cohorts of around 5,000 individuals with either binary (WTCCC) or quantitative (NFBC1966) traits, we demonstrated its power gain at the low-effect end of the genetic etiology spectrum. In aggregate, the additional low-effect variants detected by edLMM substantially improved estimation of missing heritability. edLMM moves precision medicine forward by accurately detecting the contribution of low-effect genetic variants to human diseases.

genetics↗

Exploring Nonlinear Dynamics In Brain Functionality Through Phase Portraits And Fuzzy Recurrence Plots

AO_SCPLOWBSTRACTC_SCPLOWMuch of the complexity and diversity found in nature is driven by nonlinear phenomena, and this holds true for the brain. Nonlinear dynamics theory has been successfully utilized in explaining brain functions from a biophysics standpoint, and the field of statistical physics continues to make substantial progress in understanding brain connectivity and function. This study delves into complex brain functional connectivity using biophysical nonlinear dynamics approaches. We aim to uncover hidden information in high-dimensional and nonlinear neural signals, with the hope of providing a useful tool for analyzing information transitions in functionally complex networks. By utilizing phase portraits and fuzzy recurrence plots, we investigated the latent information in the functional connectivity of complex brain networks. Our numerical experiments, which include synthetic linear dynamics neural time series and a biophysically realistic neural mass model, showed that phase portraits and fuzzy recurrence plots are highly sensitive to changes in neural dynamics and can also be used to predict functional connectivity based on structural connectivity. Furthermore, the results showed that phase trajectories of neuronal activity encode low-dimensional dynamics, and the geometric properties of the limit-cycle attractor formed by the phase portraits can be used to explain the neurodynamics. Additionally, our results showed that the phase portrait and fuzzy recurrence plots can be used as functional connectivity descriptors, and both metrics were able to capture and explain nonlinear dynamics behavior during specific cognitive tasks. In conclusion, our findings suggest that phase portraits and fuzzy recurrence plots could be highly effective as functional connectivity descriptors, providing valuable insights into nonlinear dynamics in the brain. SignificanceHere we report that phase trajectories and fuzzy recurrence plots can serve as descriptors of nonlinear functional dynamics networks. Both metrics are highly sensitive to variations in neural signals and are powerful tools for capturing distinct patterns from brain signals, making brain fingerprinting possible. This has significant implications for understanding brain state dynamics through phase trajectories and fuzzy recurrence plots, as both metrics are effective in identifying nonlinear dynamics patterns.

neuroscience↗

Exploiting the therapeutic vulnerability of IDH-mutant gliomas with zotiraciclib

Isocitrate dehydrogenase (IDH)-mutant gliomas have distinctive metabolic and biological traits that may render them susceptible to targeted treatments. Here, by conducting a high-throughput drug screen, we pinpointed a specific susceptibility of IDH-mutant gliomas to zotiraciclib (ZTR). ZTR exhibited selective growth inhibition across multiple IDH-mutant glioma in vitro and in vivo models. Mechanistically, ZTR at low doses suppressed CDK9 and RNA Pol II phosphorylation in IDH-mutant cells, disrupting mitochondrial function and NAD+ production, causing oxidative stress. Integrated biochemical profiling of ZTR kinase targets and transcriptomics unveiled that ZTR-induced bioenergetic failure was linked to the suppression of PIM kinase activity. We posit that the combination of mitochondrial dysfunction and an inability to adapt to oxidative stress resulted in significant cell death upon ZTR treatment, ultimately increasing the therapeutic vulnerability of IDH-mutant gliomas. These findings prompted a clinical trial evaluating ZTR in IDH-mutant gliomas towards precision medicine (NCT05588141). HighlightsO_LIZotiraciclib (ZTR), a CDK9 inhibitor, hinders IDH-mutant glioma growth in vitro and in vivo. C_LIO_LIZTR halts cell cycle, disrupts respiration, and induces oxidative stress in IDH-mutant cells. C_LIO_LIZTR unexpectedly inhibits PIM kinases, impacting mitochondria and causing bioenergetic failure. C_LIO_LIThese findings led to the clinical trial NCT 05588141, evaluating ZTR for IDH-mutant gliomas. C_LI

cancer biology↗