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Cheng, X.

Publications and source records attributed to Cheng, X..

At least 55 records · Page 3Linked to original sources

A Unified Mechanism for Depth Perception and Figure-Ground Organization

Understanding how the visual system unifies depth perception and figure-ground organization remains a central challenge in vision science. Stereoscopic disparity and border ownership have long been treated as distinct processes, yet both arise with similar timing in area V2 and exhibit strikingly parallel properties. Here we propose a unified mechanism that integrates both within a single hierarchical framework. Building upon the layered disparity representation introduced in our prior work, we show that border ownership--serving as the key component of figure- ground organization--emerges intrinsically from thresholded relative-disparity differencing, providing a unified basis for contour-based segmentation and depth perception. Using biologically constrained network models (TcNet), we demonstrate that this mechanism generalizes across binocular and illusory depth domains, bridging physical and non-epipolar disparity cues. At the systems level, we identify complementary dual feedback pathways from area V4: V4[->]V1, which refines and re-weights layered disparity maps, and V4[->]V2, which integrates global contextual priors such as shape continuity and category consistency. Together, these recurrent loops balance fine-scale depth precision with large-scale figure-ground coherence, offering a unified explanation for perceptual alternations such as the Rubin Face-Vase and Kanizsa illusions. This framework integrates intrinsic disparity computation, border-ownership dynamics, and hierarchical feedback modulation into a coherent, biologically plausible model. It provides a mechanistic account of how early visual areas interact with higher cortical feedback to achieve stable yet flexible perception of depth and figure-ground organization within a unified temporal cycle.

neuroscience↗

Agonism of mosquito and human transient receptor potential ankyrin 1 (TRPA1) channels by the natural drimane sesquiterpene cinnamodial

TRPA1 channels are multi-modal receptors in animals for sensing noxious physical and chemical factors. They are considered promising biochemical targets for developing repellents of arthropod disease vectors and drugs to treat a variety of medical conditions including pain, inflammation, and itch. Recently, we discovered that cinnamodial (CDIAL), a natural drimane sesquiterpene produced by the medicinal plant Cinnamosma fragrans, agonizes mosquito TRPA1 channels and is antifeedant and repellent to Aedes aegypti. However, the selectivity of CDIAL for mosquito vs. human TRPA1 and how CDIAL binds to TRPA1 channels are unknown. Here we characterize the agonism by CDIAL of Aedes aegypti (Aa) and Homo sapiens (Hs) TRPA1 channels and compare it to that induced by two other known TRPA1 agonists, nepetalactone and JT010. Heterologous expression of AaTRPA1 and HsTRPA1 in Xenopus laevis oocytes revealed that CDIAL agonized both channels with similar potency. Nepetalactone was less potent of an agonist than CDIAL for both AaTRPA1 and HsTRPA1, but was a more specific agonist for AaTRPA1 over HsTRPA1 compared to CDIAL. JT010 did not detectably activate AaTRPA1, but was a more potent agonist of HsTRPA1 than CDIAL. To generate insights into a putative binding site of CDIAL on AaTRPA1 we mutated six Lys residues (656, 678, 681, 728, 738, 744) and/or a Cys residue (684) in the coupling domain previously hypothesized to be involved. Simultaneous mutation of the six Lys residues to Ala dampened agonistic responses of AaTRPA1 to CDIAL, whereas changing Cys684 to Ser had no detectable impact. Protein modeling and molecular docking simulations for both AaTRPA1 and HsTRPA1 suggest species-specific CDIAL-binding mechanisms to the coupling domain, which involve Lys681 in AaTRPA1 and Cys621 in HsTRPA1.

pharmacology and toxicology↗

Revealing the antibiotic resistome in the global hadal trenches by large-scale cultivation and metagenomics

The global hadal trenches that reside more than 6000 meters below the sea level, represent one of Earths most remote ecosystems, potentially harboring a microbial reservoir for antibiotic resistant bacteria (ARB) and antibiotic resistance genes (ARGs). However, the global hadal environments remain the least investigated ecosystem for ARB/ARG compositions and distribution. This study took three-fold approaches to investigate the ARB/ARGs in the global hadal trench sediments, i.e., large-scale cultivation to isolate and verify ARB/ARGs from Challenger Deep sediments, metagenomic analysis of sediment samples from Challenger Deep over a six-year period, and comparative study of resistomes across six hadal trenches through metagenomic analysis. The Challenger Deep sediments had a consistent average ARG abundance of 0.02 copy/cell over a six-year period, whereas some ARG subtypes fluctuated and showed distinct temporal dynamics. Large-scale screening of ARB via microbial cultivation using 13 classes of antibiotics led to enriching distinct ARB, for which eleven genera were identified by metagenomic sequencing as major host for ARGs. The global hadal trench sediments showed a variable ARG abundance, which was significantly lower than those from environments in proximity to human activities, representing a relatively pristine reservoir. Phylogenetic analysis suggested the hadal ARGs underwent niche-specific selections and formed hadal trench-specific clusters that diverged from human-associated lineages, which can be outward transported when disturbed. The study established the hadal trench sediments, as a relatively pristine reservoir of natural ARGs, providing a crucial environmental baseline for assessing their impacts on the ecosystems and public health risks.

microbiology↗

Structure of human lymphoid-specific helicase HELLS in its autoinhibitory state

Helicase, Lymphoid Specific (HELLS), also known as Lymphoid-Specific Helicase (LSH), is a member of the SNF2 chromatin-remodeling family that regulates DNA methylation and heterochromatin organization. Unlike most chromatin remodelers, HELLS is catalytically inactive in its apo form and requires the DNA-binding protein CDCA7 for activation, though the underlying mechanism has remained unclear. Here, we combine biochemical, biophysical and cryo-electron microscopy analyses to define the structural basis of HELLS autoinhibition. HELLS alone assembles into a hexameric (trimer of dimers) architecture stabilized by interactions between its N-terminal coiled-coil (CC) domain and ATPase Lobe-1, while ATPase Lobe-2 remains flexible and disengaged. The CC domain functions both as an oligomerization scaffold and as an autoinhibitory module that restricts catalytic activity. Binding of CDCA7 and DNA promotes formation of an active HELLS-CDCA7-DNA ternary complex. CDCA7 recognizes hemimethylated CpG dinucleotides in both B-form and non-B-form DNA and stimulates HELLS ATPase activity. Together, these findings reveal the mechanism of HELLS autoinhibition and its activation by CDCA7 and DNA, providing new insight into how the HELLS-CDCA7-DNA ternary complex maintains DNA methylation and heterochromatin integrity. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=78 SRC="FIGDIR/small/692698v1_ufig1.gif" ALT="Figure 1"> View larger version (26K): org.highwire.dtl.DTLVardef@106b73borg.highwire.dtl.DTLVardef@1e7b33aorg.highwire.dtl.DTLVardef@a7be6eorg.highwire.dtl.DTLVardef@c75a5b_HPS_FORMAT_FIGEXP M_FIG C_FIG O_LIHELLS alone assembles into an inactive hexameric trimer-of-dimers C_LIO_LIThe N-terminal coiled-coil mediates oligomerization C_LIO_LICDCA7 and DNA binding activate the HELLS-CDCA7-DNA complex C_LIO_LIThe complex recognizes hemimethylated CpG in non-B-form DNA C_LI

molecular biology↗

Gut metabolite IPA alleviates white matter injury post-ICH by enhancing myelin debris phagocytosis via Stap1 inhibition

BackgroundIntracerebral hemorrhage (ICH) causes neurological dysfunction and white matter injury (WMI) characterized by myelin loss, axonal injury and myelin debris accumulation. Microglia-mediated debris clearance is critical for WMI repair. The microbiota-gut-brain axis plays an essential role in the central nervous system diseases, one of the ways in which gut microbiota affects brain is via producing metabolites. Indole-3-proprionic acid (IPA), a tryptophan-derived metabolite that mainly produced by Clostridium sporogenes, exhibits anti-inflammatory and neuroprotective properties. However, its effect on ICH remains unclear. This study aims to investigate the IPA level after ICH and the therapeutic effects of IPA on neurological deficits and WMI, as well as the potential mechanisms underlying IPA-mediated neuroprotection. MethodsAn ICH model was established using C57BL/6 mice, which then received intragastric IPA (20 mg/kg/day). Fecal abundance of IPA-related genes and IPA levels in feces and plasma were measured by qPCR and UPLC-MS/MS. Behavioral tests, qPCR, and immunofluorescence staining were used to assess neurological function, myelin integrity, and axonal injury. In vitro, BV2 microglia, with or without Stap1 knockdown, were co-cultured with myelin debris to assess IPAs effects on phagocytosis. Additionally, targeted plasma IPA profiling was performed in 30 ICH patients and 30 matched healthy controls. ResultsThe relative abundance of IPA production-related genes and IPA levels in feces and plasma were significantly decreased after ICH and remained low into the chronical phase. After IPA administration, the neurological deficits, myelin loss and axonal injury of mice with ICH were significantly improved. In vitro, IPA increased BV2 microglia myelin debris phagocytosis by inhibiting Stap1 expression. IPA levels were significantly reduced in ICH patients, consistent with ICH mouse model. ConclusionsOur findings demonstrated that the gut microbiota-derived metabolite IPA could facilitate neurological deficits recovery and alleviate WMI, which could be a promising therapeutic strategy to improve ICH prognosis.

neuroscience↗

Drosophila Sociality Influences Immune Peptide Load and Apoptosis-induced Tumor Suppression independently of the Antitumor Peptide Defensin

Patients social environment might influence cancer outcome. This potentially happens in Drosophila, as we previously reported that the social context influences the growth of intestinal tumors. To uncover the underlying social-induced physiological mechanisms, we performed RNA-seq of isogenized beheaded tumorous Drosophila. Importantly, expression of several immune peptides varied according to the social-induced tumor growth effect. Furthermore, ectopic expression in tumors of the apoptotic-inhibitor p35 suppressed the social-induced effect. Next, we challenged the immune peptide Defensin, previously reported to suppress imaginal disc tumor growth through a cell-death/JNK-dependent network. Nonetheless, the social-induced tumor suppression was maintained upon Defensin overexpression or JNKK-knockdown in tumors, and in defensin mutants. Surprisingly, tumor growth was reduced in the latter, indicating that Defensin sustains the growth of these intestinal tumors. In summary, our study indicates that the social context affects the immune response and that a given immune peptide may have opposite effects depending on tumor type.

cancer biology↗

MSACLR: Contrastive Learning of Protein Conformations from MSAs

We propose MSACLR (Multiple Sequence Alignment Contrastive Learning Representation), a two-stage contrastive learning framework that maps MSA space to conformational space. In Stage 1, embeddings are trained to discriminate structural folds across diverse proteins using only MSA information. In Stage 2, embeddings are fine-tuned on subMSAs labeled by their associated predicted structural clusters, enabling discrimination of alternative conformations within the same protein. To enrich training data, we introduce BLOSUM62-guided [1] augmentation, which expands the pool of subMSAs associated with each structural cluster label by introducing sequence-level diversity. Our experiments show that MSACLR embeddings achieve clearer fold-level separation than single-sequence baselines, while fine-tuned embeddings capture conformational variation across scales--from local loop motions to domain motions and fold switching. MSACLR provides a foundation for efficient exploration of MSA space and enables sampling of conformational ensembles, bridging the gap between static structure prediction and dynamic protein behavior.

bioinformatics↗

SpaPheno: Linking Spatial Transcriptomics to Clinical Phenotypes with Interpretable Machine Learning

Linking spatial transcriptomic data to clinically relevant phenotypes is essential for advancing spatially informed precision oncology. Here, we present SpaPheno, an interpretable machine learning framework that integrates spatial transcriptomics with clinically annotated bulk RNA-seq to identify spatially resolved biomarkers predictive of patient outcomes, including survival, tumor stage, and immunotherapy response. SpaPheno provides multi-scale interpretability from tissue regions to cell types and individual spatial spots, enabling clear biological insights from complex spatial data. We validate SpaPheno through extensive simulations and applications to multiple cancer cohorts--primary liver cancer, clear cell renal cell carcinoma, breast cancer, and melanoma--demonstrating robust predictive performance alongside biologically meaningful spatial patterns. SpaPheno offers a generalizable strategy to translate spatial omics data into clinically actionable knowledge, facilitating precision oncology informed by tumor spatial architecture.

bioinformatics↗

Hyperbolic Wavelet Interaction Network (HyWinNet): Multi-Scale Geometric Learning for Interpretable Protein-Protein Interaction Prediction

Understanding the multi-scale organization of protein-protein interactions (PPIs) is fundamental to deciphering cellular signaling, allosteric regulation, and disease mechanisms, yet existing computational approaches fail to simultaneously resolve atomic-scale binding interfaces and pathway-level coordination. We present HyWinNet, a geometric deep learning framework that unifies Lorentzian hyperbolic graph neural networks with spectral graph wavelet transforms to intrinsically model the hierarchical architecture of biological interactions. The core innovation lies in three synergistic components: (1) Hyperbolic embeddings that preserve evolutionary-conserved topological relationships through negatively curved space projections, capturing scale-free properties of protein networks; (2) Multi-scale wavelet decomposition operating at biologically grounded resolutions to jointly analyze local residue contacts and global pathway dynamics; (3) Contrastive learning with stochastic feature dropout that mimics natural binding interface plasticity. Benchmarked against state-of-the-art methods, HyWinNet demonstrates superior performance in recovering known interactions while predicting previously unannotated functional sites validated through independent structural and biochemical studies. By bridging hyperbolic geometry with graph signal processing, this work establishes a new paradigm for analyzing multi-scale biological networks, offering both interpretable computational predictions and testable hypotheses for experimental validation. The frameworks ability to map hierarchical relationships from atomic details to system-level modules provides a transformative tool for drug discovery and mechanistic studies of complex diseases.

bioinformatics↗

Time-resolved structures of β2-adrenergic receptor modulation by a photoswitchable beta-blocker

G protein-coupled receptors (GPCRs) regulate essential physiological responses and are important drug targets, yet their ligand-induced conformational dynamics remain poorly understood. The {beta}2-adrenergic receptor ({beta}2AR) is a prominent member of the GPCR family. It regulates bronchial and vascular function and is a significant drug target, particularly in respiratory and smooth muscle-related disorders. We employed time-resolved crystallography at X-ray free-electron lasers (XFELs) to capture the conformational dynamics of {beta}2AR bound to photoazolol-1, a beta-blocker derivative developed for photopharmacological applications. Structural snapshots of the receptor bound to trans-photoazolol-1 (pre-photoconversion), a strained intermediate, and the fully photoisomerized cis-photoazolol-1 reveal an intricate interplay between ligand chemistry and receptor plasticity. Isomerization of the azobenzene moiety induces distinct conformational changes within the orthosteric pocket, altering interactions with the extracellular loop 2 and transmembrane helices 5 and 6. Supported by functional assays, these structural shifts suggest that photoazolol-1 transitions from an inverse agonist to a neutral antagonist upon photoactivation. Our findings uncover a mechanism of GPCR modulation reminiscent of rhodopsin activation and offer a framework for designing ligands that harness light-driven transitions to achieve spatiotemporal control of receptor function.

biochemistry↗

Inhibition of Clostridioides difficile-specific DNA adenine methyltransferase CamA by analogs of S-adenosyl-L-methionine

Epigenetically-targeted therapies, especially those inhibiting S-adenosyl-L-methionine (SAM)- dependent methylations of DNA, mRNA and histones, have advanced rapidly in cancer treatment. However, these therapies remain underexplored for antibiotic development, despite the growing threat of antimicrobial resistance. Here, we screened a focused library of SAM analogs against the DNA adenine methyltransferase CamA specific to the enteric pathogen Clostridioides difficile. At the same time, we examined six other adenine methyltransferases, including two bacterial DNA methyltransferases, and four human RNA methyltransferases having distinct RNA substrates. Compound 113 selectively inhibited CamA (IC50 = 0.15 M). In addition, compound 67 inhibited Caulobacter crescentus CcrM (IC50 = 1.8 M), which has orthologs present in pathogens such as Brucella; while compounds 77 and 37 inhibited the human DNA methyltransferase complexes MettL3-MettL14 and MettL5-Trm112, respectively, at 7-8 M concentrations. These results provide chemical probes for exploring the role of CamA in sporulation and colonization, with potential as antivirulence agents against C. difficile infection. Our study also introduces the first chemical probes for inhibiting bacterial CcrM and human MettL5, each of which plays key roles in their respective hosts. Table of Contents Graphic (TOC) O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=163 SRC="FIGDIR/small/670177v1_ufig1.gif" ALT="Figure 1"> View larger version (15K): org.highwire.dtl.DTLVardef@f7d56org.highwire.dtl.DTLVardef@edbd09org.highwire.dtl.DTLVardef@15abc9org.highwire.dtl.DTLVardef@c12ca7_HPS_FORMAT_FIGEXP M_FIG C_FIG

biochemistry↗

bacNeo: a computational toolkit for bacteria-derived neoantigen identification

Intratumour microbiome can restore anti-tumour immunity with bacterial peptides potentially serving as neoantigens, while robust in-silico tools for bacterial neoantigen identification remain lacking. We developed bacterial neoantigen (bacNeo), a multi-omics based computational toolkit that contains three modules to classify bacterial taxonomy, identify host HLA alleles, and predict bacterial neoantigens. bacNeo could enable personalised neoantigen discovery to advance therapeutic strategies across diverse cancer types.

bioinformatics↗

HER2; p53 Co-mutated Cancers Show Increased Histone Acetylation and are Sensitive to Neratinib plus Trastuzumab Deruxtecan.

In metastatic breast cancer, HER2-activating mutations often co-occur with TP53 mutations, a combination linked to poor response to neratinib and worse prognosis. To model this clinical challenge, we bred HER2 V777L transgenic mice with two TP53 mutant alleles: TP53 R172H (the murine homolog of human TP53 R175H) and TP53fl/fl, which mimics p53 truncations common in human tumors. TP53 mutations accelerated tumor development and reduced survival in HER2-mutant mice. These co-mutant tumors were resistant to neratinib but remained sensitive to exatecan, the topoisomerase I (TOP1) inhibitor payload in trastuzumab deruxtecan (T-DXd). Mechanistically, TP53 mutant tumors exhibited upregulation of histone acetylation, hypertranscription of DNA repair factors, increased chromatin accessibility, and rendered cells more susceptible to TOP1 inhibitors via G2/M arrest and apoptosis. This vulnerability is dependent on transcriptional activity of TP53 mutations, highlighting a novel strategy to treat HER2;TP53 co-mutant breast cancers using TOP1-targeted therapies. Statement of SignificanceTP53 mutations sensitize HER2-mutant cancers to TOP1 inhibitors via chromatin accessibility and hyper-transcription, supporting combination therapy with neratinib and T-DXd in TP53/HER2 co-mutant breast cancers.

cancer biology↗

Discovery of Niclosamide Analogs with Potent Mitochondrial Uncoupling Activity with reduced toxicity

Mitochondrial uncouplers have shown clinical potential across various diseases, including cancer. Niclosamide, an FDA-approved anthelmintic drug, acts as a mild mitochondrial uncoupler and has demonstrated anticancer activity in multiple preclinical cancer models. However, its clinical application remains limited, with some attributing this to poor bioavailability, while the underlying mechanisms are still unclear. Here, we demonstrate that niclosamide exhibits a dose-dependent biphasic effect, promoting uncoupling at low concentration while acting as a mitochondrial inhibitor at high concentration, which could restrict its therapeutic window and limit efficacy. To overcome this challenge, we aimed to develop next-generation mitochondrial uncouplers (MUs) by synthesizing and evaluating novel Niclosamide derivatives with enhanced therapeutic potential. Through structural modifications, we optimized uncoupling activity while reducing inhibitory toxicity, thereby expanding the pharmacological window. Our findings suggest that fine-tuning the molecular structure of mitochondrial uncouplers could provide a safer and more effective metabolic reprogramming strategy for cancer treatment.

pharmacology and toxicology↗

AIDO.Tissue: Spatial Cell-Guided Pretraining for Scalable Spatial Transcriptomics Foundation Model

Single-cell spatial transcriptomics enables high-resolution insights into tissue organization and cell-cell interactions, yet poses significant computational and modeling challenges due to its scale and complexity. Here we introduce AIDO.Tissue, a spatially-informed pretraining framework. The design employs multiple cells as input and an asymmetric encoder-decoder architecture, making it effectively encodes cross-cell dependencies while scaling to large data. Systematic evaluation shows that our method scales with neighboring size and achieves state-of-the-art performance across diverse downstream tasks, including spatial cell type classification, cell niche type prediction and cell density estimation. These results highlight the importance of spatial context in building general-purpose foundation models for tissue-level understanding.

bioinformatics↗

Structural and Functional Mechanisms Underlying Activation Gate Dynamics and IFM Motif Accessibility in Human Nav1.5

Voltage-gated sodium channels are vital for regulating excitability in muscle and nerve cells, and their dysregulation is linked to a range of diseases. However, therapeutic targeting of Nav channels remains challenging due to a limited understanding of their gating mechanisms. Here, we present a cryo-EM structure of human Nav1.5 in an intermediate open state, stabilized by interactions between the N-terminal domain and the S6I segment. This structure reveals a previously uncharacterized Na+ binding site adjacent to the conserved inactivation (IFM) motif. Molecular dynamics simulations demonstrate that monovalent cations stably occupy this site, while electrophysiological recordings demonstrate that ion binding modulates IFM motif docking and fast inactivation kinetics. Our findings reveal that IFM accessibility is dynamically regulated in this intermediate state, challenging the canonical hinged-lid model of fast inactivation. Collectively, our study provides a revised structural framework for Nav1.5 gating mechanisms, suggesting an alternative pathway for ion accessibility that may inform better mechanistic and therapeutic strategies for treating Nav1.5-related cardiac arrhythmias.

biophysics↗

Intestinal Epithelial C/EBPβ Deficiency Impairs Colitis-Associated Tumorigenesis by Disrupting CXCL1 /CXCL2/CXCL5-CXCR2-Mediated Neutrophil Infiltration

Dysregulated transcription factors critically link chronic inflammation to oncogenesis in colitis-associated colorectal cancer (CAC), but their mechanistic roles remain incompletely understood. By integrating microarray and transcriptome sequencing data from ulcerative colitis (UC), colitis-associated cancer (CAC), and colorectal cancer (CRC) patients, we identify C/EBP{beta} as a key transcriptional regulator whose elevated expression inversely correlates with survival. In azoxymethane (AOM)/dextran sulfate sodium (DSS)-induced CAC models, intestinal epithelial C/EBP{beta} is upregulated during tumor progression, correlating with exacerbated tumor burden and neutrophil infiltration. Mice with intestinal epithelial-specific Cebpb deletion (Cebpb{Delta}IEC) show resistance to carcinogenesis, accompanied by reduced neutrophil infiltration and tumor growth. Mechanistically, C/EBP{beta} transcriptionally activates CXCR2 ligands (CXCL1, CXCL2, and CXCL5) to drive neutrophil recruitment. Pharmacological inhibition of CXCR2 phenocopies the anti-tumor effects of Cebpb{Delta}IEC deletion, further validating this axis as a therapeutic target. Correlation analysis in patient tissues confirms positive relationships between C/EBP{beta}, CXCR2 ligands, and neutrophil infiltration, suggesting that targeting the C/EBP{beta}-CXCL1/2/5-CXCR2 axis may offer a novel strategy for CAC treatment.

cancer biology↗

Cerebellum metastasis model of HER2-positive breast cancer unveils key role of IL34-induced Arg1+ macrophages.

Brain metastases occur in up to 40% of Stage IV breast cancer patients. The cerebellum is a frequent location for metastases in HER2-positive breast cancer patients, but the mechanisms for this are unknown. Here, we developed a syngeneic, immunocompetent mouse model for breast cancer brain metastases by stereotactically injecting mouse HER2-overexpressing breast cancer organoids into the cerebellum. Growth of these cerebellar metastases was monitored by MRI and trastuzumab optical imaging using a near-infrared fluorophore conjugated to trastuzumab. Spatial transcriptomics identified interleukin-34 production by breast cancer cells inducing ARG1+ macrophages at the invading edge of the metastasis. Treatment with a blocking antibody to interleukin-34s receptor, CSF1R, produced tumor shrinkage. These findings have immediate translation potential as a CSF1R-blocking antibody is FDA-approved. Further, it demonstrates that cancer-associated inflammation bordering the brain metastasis promotes metastatic growth and offers a molecularly targeted strategy to treat inflammation in brain metastasis. Graphical summary O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=200 SRC="FIGDIR/small/660224v1_ufig1.gif" ALT="Figure 1"> View larger version (38K): org.highwire.dtl.DTLVardef@9f1a50org.highwire.dtl.DTLVardef@178acc5org.highwire.dtl.DTLVardef@196d803org.highwire.dtl.DTLVardef@3fe631_HPS_FORMAT_FIGEXP M_FIG C_FIG

cancer biology↗