Biology subjects

Chen, Z.

Publications and source records attributed to Chen, Z..

At least 145 records · Page 8Linked to original sources

bioRxiv2026

Multi-omics analysis of the potential of MACC1 as a biomarker and therapeutic target for colonic adenocarcinoma

Colonic adenocarcinoma (COAD) is a major cause of cancer-related mortality worldwide. Various tumors are linked to metastasis-associated in colon cancer 1 (MACC1). This study aimed to analyze public datasets to examine MACC1 expression, signaling pathways, copy number variations, and associations with immune cell subsets in COAD employing bioinformatics. MACC1 expression was elevated in COAD, especially in Wnt signaling and chromatin modifier pathways. Analysis of somatic copy number alterations in The Cancer Genome Atlas-COAD dataset revealed a link between MACC1 and DNA damage repair. MACC1 also showed a negative correlation with genes involved in immune cell infiltration in patients with COAD, including cluster of differentiation (CD)8+ T cells, activated dendritic cells, CD8 T cells, and cytotoxic cells. Collectively, these findings suggest MACC1 as a potential prognostic biomarker and therapeutic target for COAD.

cancer biology↗

bioRxiv2026

Dynamic genomes uncover opposite sex determination in the invasive quagga and zebra mussels

Sex determination is a fundamental developmental switch, yet the genetic architectures that underlie transitions between sex-determining systems remain poorly understood, especially in non-model animals with homomorphic sex chromosomes. Here, we combine chromosome-scale genomes, whole-genome resequencing of 80 sexed individuals, sex-specific k-mer analyses, and developmental transcriptomics to resolve and compare sex determination in zebra and quagga mussels, two closely related and globally invasive freshwater bivalves. We find that these species have evolved sharply contrasting sex-determining architectures since their divergence. Zebra mussels show signatures of a polygenic ZZ/ZW system, with sex-linked regions on multiple chromosomes, including signal at the conserved ovarian regulator FoxL2. In contrast, quagga mussels possess a localized [~]800 kb XX/XY sex-determining region containing FoxL2-Y, a duplicated and structurally modified FoxL2 paralog and candidate male-determining locus. In quagga mussels, SNP-based differentiation, model-based inference, sex-biased read coverage, and male-specific k-mers independently converge on this Y-linked region, while diagnostic k-mer screening of staged embryonic transcriptomes reveals rare, early developmental expression of FoxL2-Y, consistent with a transient regulatory role. The quagga sex-determining region is enriched for C-type lectins and other genes implicated in reproductive interactions, suggesting that haploid selection may have contributed to the stabilization of this region. Together, these findings show that closely related species can rapidly evolve different genetic solutions to sex determination and identify gene duplication, genome dynamism, and reproductive selection as potential contributors to sex-determining system turnover. Because zebra and quagga mussels are major freshwater invaders, resolving their divergent reproductive architectures also provides essential genomic context for assessing the future feasibility of sex-ratio-based biocontrol strategies.

genomics↗

bioRxiv2026

A FZD4/LRP5 agonist restores pericyte coverage and vascular integrity by increasing PDGFB signaling

Pericytes, specialized mural cells of capillaries, fulfill crucial physiological functions including promoting endothelial barrier function and regulating angiogenesis. Pericyte loss or dysfunction represents a central pathological feature in diabetic retinopathy (DR) and is increasingly recognized in neurodegenerative diseases as well as in poor stroke outcomes, underscoring an urgent need for therapies that restore pericyte function or promote their regeneration. Here, we utilized a Frizzled4 (FZD4) and Low-Density Lipoprotein Receptor-Related Protein 5 (LRP5) agonist antibody (F4L5.13) to investigate the functional consequences of mimicking {beta}-catenin-dependent signaling in CNS endothelial cells (ECs), which is physiologically induced by Norrin or WNT7A/B. In platelet-derived growth factor subunit B (Pdgfb) EC-specific knockout (ECKO) mice, a model of severe developmental pericyte deficiency with secondary blood-retina barrier (BRB) defects and hemorrhages, F4L5.13 significantly promoted retinal pericyte/mural cell proliferation and coverage, improved BRB function, reduced hemorrhages, and normalized vascular morphology. F4L5.13 restored Pdgfb mRNA expression levels from non-recombined cells in Pdgfb ECKO retinas. These findings highlight interactions of {beta}-catenin-dependent signaling and PDGFB production, identify a key pharmacodynamic action of F4L5.13 distinct from anti-VEGF therapies, and suggest that FZD4/LRP5 agonists may have uses as a regenerative pharmacology approach that promotes pericyte coverage in the neurovascular unit.

developmental biology↗

bioRxiv2026

Saxiphilin is a broad-spectrum toxin sponge for C13-modified saxitoxins

Saxitoxin (STX) and its congeners (paralytic shellfish toxins, PSTs) are among the most potent small-molecule toxins. PSTs are produced by harmful algal blooms and derive toxicity by disrupting voltage-gated sodium channel (NaV) bioelectrical signaling. Understanding how PST structural variation affects target binding is crucial to develop means to counteract PSTs and exploit these natural products as drug development leads. Frog and toad saxiphilins (Sxphs) are soluble, high-affinity STX toxin sponge proteins that offer a powerful platform to define PST-protein interactions. Here, we show that American bullfrog (Rana catesbeiana) RcSxph and High Himalaya frog (Nanorana parkeri) NpSxph bind a broad set of C13-modified STX congeners. High-resolution X-ray crystal structures of toxin complexes with RcSxph, RcSxph mutants, and NpSxph unveil two C13-aryl congener binding modes, termed compact and open, that depend on the RcSxph Tyr558 local environment. These results highlight a remarkable adaptability of Sxphs for accommodating chemically diverse STX analogs and reveal unexpected toxin conformational plasticity. These findings have implications for understanding PST interactions with biological targets and informing design of STX-based probes and NaV modulators.

biophysics↗

bioRxiv2026

Fluorescence anisotropy structured illumination microscopy for quantitative super-resolved mapping of cell microenvironment and cytoskeletal dynamics

The crowded intracellular milieu shapes organelle architecture and dynamics, yet nanoscale heterogeneity in its physicochemical properties remains difficult to visualize with conventional fluorescence anisotropy (FA) imaging. Here, we develop fluorescence anisotropy structured illumination microscopy (FA-SIM), which employs orthogonal-polarization structured illumination with dual-angle detection to achieve [~]100-nm resolution and quantitative FA retrieval with 0.56% relative error, representing over 20-fold higher accuracy than conventional FA imaging. With low phototoxicity, FA-SIM enables dual-color, hour-long quantitative super-resolution imaging in cells. Using viscosity standards, defined nanoparticles and small-molecule drug binding assays, we validate FA-SIM as a quantitative reporter of rotational mobility and molecular interactions. In cells, FA-SIM resolves nanoscale crowding heterogeneity, correlates anisotropy landscapes with condensate dynamics, and uncovers a radial crowding gradient across the microtubule network and mitotic spindle. Long-term dual-color imaging further resolves coordinated actin-microtubule remodeling and associated microenvironmental changes. By enabling quantitative, super-resolved mapping of intracellular physical properties in living systems, FA-SIM provides a powerful platform for investigating the physical regulation of cellular organization and dynamics in health and disease.

cell biology↗

bioRxiv2026

Co-evolution of Oncogenic KRAS Signaling and LILRBhigh Macrophages Drives Pancreatic Cancer Recurrence

Pancreatic ductal adenocarcinoma (PDAC) frequently recurs after surgical resection, indicating that residual disease is sustained by coordinated tumor-microenvironment interactions. To define the biological basis of recurrence, we leverage large-scale clinical data from 2,710 patients, deeply characterized multi-omics profiling (whole-exome, bulk RNA, and single-nucleus sequencing) of 36 matched primary and locally recurrent PDACs, an in-house multiplex spatial imaging cohort of 190 patients, and extensive public datasets. Recurrent tumors were characterized by increased KRAS mutant allele dosage and reinforced KRAS signaling, accompanied by expansion of basal-like malignant cell states. In parallel, we identified an immunosuppressive macrophage population marked by high LILRB expression that spatially co-localized with KRAS-activated tumor cells. Functional studies showed that LILRB4+ macrophages enhanced tumor cell plasticity and progression, whereas inhibition of macrophage LILRB4 suppressed these phenotypes. Notably, a first-in-class human anti-LILRB4 antibody reduced macrophage-driven tumor traits, and dual targeting of KRAS signaling and LILRB4 achieved superior tumor control in macrophage-containing mouse models. These findings reveal a co-evolved tumor-immune niche underlying PDAC recurrence and nominate the KRAS-LILRB4 axis as a therapeutic vulnerability.

cancer biology↗

bioRxiv2026

Evolutionarily conserved neural dynamics across mice, monkeys, and humans

On evolutionary timescales, brain circuits adapt to support survival in each species ecological niche. While some anatomical aspects of neural circuitry are conserved across species with distant evolutionary origins, each species also exhibits specific circuit adaptations that enable its behavioral repertoire. It remains unclear whether homologous brain regions leverage analogous neural computations as different species perform common behaviors such as reaching and manipulating objects. Here, we directly assessed conservation of neural computations using intracortical recordings from mouse, monkey, and human motor cortex--a homologous region across many mammals--during motor behaviors crucial for survival. We hypothesized that, despite their phylogenetic distance, rodents and primates produce movements through conserved neural computations implemented by motor cortical population dynamics. Remarkably, we found that movement-related neural dynamics were highly conserved across species, while variations in behavioral output were uniquely captured in neural trajectory geometries. Strikingly, neural dynamics during movement across species were more conserved than those across brain regions in the same human and between motor preparation and execution in the same monkeys. Lastly, through manipulation of neural network models trained to perform reaching movements, we reinforce that conservation of neural dynamics across species likely stems from shared circuit constraints. We thus assert that evolution maintains neural computations across phylogeny even as behavioral repertoires expand.

neuroscience↗

bioRxiv2026

Toward Computationally Complete Spatial Omics

Multimodal spatial omics has transformed biology by mapping molecular complexity within intact tissues, yet current technologies remain limited in the number of modalities measured simultaneously and often produce lower-quality data than single-modality assays. We present COSIE, a computational framework that generates high-resolution, multilayered molecular landscapes across tissue sections, individuals, and platforms. COSIE integrates histology, epigenome, transcriptome, proteome, and metabolome into a unified representation. Applied to 12 datasets spanning 10 spatial technologies, eight modalities, and nine tissue types, ranging from thousands of spots to millions of cells, COSIE outperforms existing methods. It resolves tissue structures, enhances noisy measurements, predicts unmeasured modalities, and captures dynamic processes. In human tumors, COSIE identifies invasive subregions linked to clinical outcomes and predicts spatial gene expression in TCGA samples using only histology images. By transforming fragmented data into comprehensive spatial maps, COSIE advances computationally complete spatial omics and the creation of digital tissue twins for biomedicine.

genomics↗

bioRxiv2026

Streak-Aware Localization Microscopy Enables High-Throughput Brain Imaging Across Platforms

Optical, ultrasound, and optoacoustic localization microscopy based on microparticle tracking has enabled surpassing the resolution limits imposed by ultrasound diffraction and optical diffusion in tissues. However, its reliance on high-speed (kilohertz) data acquisition systems for precise emitter localization and tracking substantially increases methodological complexity and data storage demands, limiting scalability and applicability beyond specialized benchtop platforms. Here, we present streak-aware localization microscopy (SALM) that employs localization- and tracking-free deep learning model to convert motion-blurred streaks originating from low frame rate recordings of flowing emitters into super-resolved structural and functional readouts. In optical implementations, SALM exploits streaks captured by low-speed cameras to recover capillary-level cerebrovascular maps across a variety of benchtop, miniaturized, and second near-infrared preclinical imaging platforms, achieving over 30-fold reduction in the reconstruction time compared to conventional localization pipelines. We further introduce three coded excitation strategies that embed finer time-varying vectorial flow signatures into individual streaks, enabling single-frame velocimetry and video-rate hemodynamic imaging. Extending SALM to ultrasound imaging enables high-fidelity vascular imaging with centimeter-scale penetration in rhesus macaque and rat brains while reducing plane-wave compounding frame rates by up to one order of magnitude. By overcoming long-standing trade-offs between spatiotemporal resolution and hardware complexity, SALM offers a flexible and scalable framework for next-generation super-resolution microscopy.

neuroscience↗

bioRxiv2026

Tissue- and Age-Specific Transcriptomic and Metabolomic Analysis Reveals Regulatory Mechanisms of Ginsenoside Biosynthesis in Panax notoginseng

Ginsenosides are the primary bioactive compounds in Panax notoginseng, but the transcriptional mechanisms governing their tissue- and age-dependent accumulation remain elusive. Here, we integrated targeted metabolomics with transcriptome profiling across four tissues (root, stem, leaf, and flower) and three developmental stages (1-3 years) to investigate the spatiotemporal regulation of ginsenoside biosynthesis. We observed distinct tissue- and age-specific accumulation patterns: roots exhibited a progressive increase in total ginsenoside content during the second and third years, while flowers preferentially accumulated rare protopanaxadiol-type ginsenosides such as Rg3-2. Transcriptomic analysis revealed extensive differential gene expression across tissues and stages, particularly in roots during late development. Clustering and transcription factor (TF) enrichment analyses identified multiple tissue-associated regulatory modules. Four TFs--AT3G12130, SPL9, MYB33, and SPL1--emerged as core candidates based on coordinated expression, promoter motif enrichment, and functional annotation of predicted target genes. Motif analysis further linked these TFs to key biosynthetic genes involved in triterpenoid oxidation and glycosylation, including CYP716A53v2 and CYP716A47. Together, these findings suggest that tissue-specific ginsenoside accumulation in P. notoginseng is associated with coordinated transcriptional regulation of biosynthetic enzymes. This study provides a transcriptomic framework for understanding spatial regulation in ginsenoside biosynthesis and identifies candidate regulators for future functional validation and metabolic engineering.

plant biology↗

bioRxiv2026

Multiscale confidence quantification for virtual spatial transcriptomics with UTOPIA

Virtual spatial transcriptomics (ST) methods predict gene expression or cell types from histology images, extending molecular readouts beyond the limited regions or samples directly measured by ST platforms. However, the statistical reliability of these predictions remains unclear. Here, we present UTOPIA, a model-agnostic framework for multiscale confidence quantification in virtual ST. UTOPIA assigns statistically calibrated confidence scores to predictions across spatial resolutions and biological granularities, ranging from single genes to metagenes and from specific cell types to broader cell classes. UTOPIA controls false discovery rates for detecting genes, metagenes, or cell types while accounting for local tissue context. We show that prediction confidence depends critically on both spatial resolution and biological granularity, with reliable inference often emerging only at coarser, biologically meaningful scales. Across multiple ST platforms and in both in-sample and out-of-sample settings, UTOPIA enhances interpretability, prevents false biological conclusions, and enables more trustworthy downstream analyses of virtual ST.

genomics↗

bioRxiv2026

Activation of PPARγ redirects fibro-adipogenic progenitors to replace ectopic bone with fat in models of fibrodysplasia ossificans progressiva and trauma-induced heterotopic ossification

The pathologic, osteogenic differentiation of fibroadipogenic progenitor cells (FAPs) is the primary recognized contributor to ectopic bone formation in fibrodysplasia ossificans progressiva (FOP) and trauma-induced heterotopic ossification (HO). Both conditions are characterized by up-regulated BMP signaling - the former by a gene mutation rendering the BMP receptor ACVR1 susceptible to activation by inflammatory ligands (Activin A), and the latter by up-regulated presence of BMP2 ligand in the setting of unmutated BMP receptor. We performed an unbiased assessment of FDA-approved therapies which would optimally target the transcriptional aberrations observed in developing FOP and HO lesions based on publicly-available datasets. This analysis uncovered rosiglitazone, a peroxisome proliferator-activated receptor gamma (PPAR{gamma}) agonist as the highest scoring therapeutic option across three data sets for both conditions. Rosiglitazone treatment eliminated ectopic bone lesions in a mouse model of FOP, and replaced these lesions with ectopic adipose tissue; similarly, systemic and local rosiglitazone treatment eliminated ectopic bone lesions in a mouse model of trauma-induced HO and replaced these lesions with ectopic adipose tissue. Our findings were corroborated by a single case report from 2010 showing positive results with rosiglitazone in a non-diabetic patient with FOP, with no subsequent studies. Overall, our findings suggest that a previously FDA-approved therapeutic is likely to be a successful therapeutic agent for both FOP and trauma-induced HO, both conditions for which current therapeutic options remain inadequate. One Sentence SummaryWe show that a previously FDA-approved therapeutic known to induce adipogenesis reduces ectopic bone and induces ectopic fat formation in diseases of heterotopic ossification.

cell biology↗

bioRxiv2026

Mitotic bookmarking by Prox1 preserves mammalian neuronal lineage identity memory via promoting timely H3K27me3 restoration

Mitosis poses a daunting challenge to transgenerational inheritance of cell identity memory. How neuronal lineage identity is faithfully transmitted across mitosis remains largely unexplored. Here we report that, in mouse hippocampus, the transcription factor Prox1 acts as a mitotic bookmark for safeguarding neuronal lineage identity across cell divisions. Prox1 exhibits mitotic retention in dentate gyrus (DG) neural stem cells and defines DG lineage identity by suppressing the alternative cornu ammonis (CA) identity. Mitotic bookmarking by Prox1 at key bivalent CA identity genes promotes timely and precise restoration of Polycomb repressive complex 2 (PRC2)-mediated H3K27me3 deposition to avoid ectopic expression of CA identity genes and lineage identity crisis. Remarkably, specific mitotic retention-deficient Prox1 conditional knock-in mice produce severe DG developmental defects. Thus, mitotic bookmarking imprints neuronal lineage identity in mouse hippocampus, which is likely to represent a fundamental principle underlying the preservation of lineage identity memory in mammalian brain development.

developmental biology↗

bioRxiv2026

Reconstructing multi-scale tissue spatial architecture from single-cell RNA-seq with REMAP

Understanding spatial organization of cells is critical for deciphering tissue function and disease. Single-cell RNA-sequencing (scRNA-seq) profiles transcriptomes at scale but loses spatial context, while spatial transcriptomics (ST) preserves spatial information but is constrained by cost and gene coverage. Here, we present REMAP, a deep learning framework that integrates gene expression with neighborhood-level gene-gene covariance to reconstruct multi-scale spatial organization of scRNA-seq data using one or multiple ST references. Across 2D and 3D mouse brain, human fetal cortex, and seven human cancer types, REMAP consistently outperformed existing approaches. Applied to a human multiple sclerosis atlas, REMAP resolved microglial neighborhood heterogeneity, and identified a rare pro-inflammatory microglia-astrocyte subpopulation. Across diverse cancers, REMAP recovered conserved spatially-defined cancer-associated fibroblast subtypes with known prognostic significance. By transforming cost-efficient single-cell datasets into spatially interpretable tissue maps, REMAP enables spatial hypothesis generation, microenvironment discovery, and population-scale inference of conserved and perturbed architectural principles in human disease.

genomics↗

bioRxiv2026

rRNA Expansion Segments Mediate Ribosome Dimerization as a Conserved Stress Response

Inhibition of mRNA translation is a common feature in proteostatic stress cellular responses. Puromycin, a widely used compound for studying translation, disrupts protein synthesis by mimicking the 3 end of aminoacyl-tRNAs. Despite its extensive use as a research tool to probe the connection between translation activity and various physiological and pathological states, the cellular response associated with puromycin-induced translation stress remains incompletely understood. Utilizing in situ cellular electron tomography and topology analysis, we visualized the translation machinery at high resolution. Our analysis revealed that puromycin-treated neuronal cells exhibit an accumulation of "idle ribosomes" characterized by the binding of eIF5A, indicating a close association of this factor with translationally inactive ribosome states under stress. Additionally, the idle ribosomes formed dimeric complexes mediated by ribosomal RNA expansion segments, suggesting an evolved mechanism involving these regions in translation hibernating and protecting idle ribosomes. We show that the hibernating disome formation is not unique to puromycin administration but represents a conserved mechanism as a response to different cellular stressors including those associated with endoplasmic reticulum (ER) stress and amino acid depletion. Altogether, our findings shed light on previously unexplored aspects regarding unique states of mammalian ribosome hibernation, and collectively offers new avenues for understanding the correlation of cellular stress response and the regulation of protein synthesis.

molecular biology↗

bioRxiv2026

Event2Flow: Scalable imaging of peripheral and cerebral hemodynamics with event-based vision sensors

Accurate blood flow mapping over mesoscale fields of view is essential for understanding physiological and pathological processes, yet conventional optical methods often rely on bulky high-speed cameras that generate massive datasets with excessive computation burden. Here, we introduce Event2Flow, a compact and data-efficient framework leveraging event-based vision sensors, which asynchronously capture brightness changes with sub-millisecond latency and minimal data redundancy. Event2Flow supports multiple contrast mechanisms for flow measurement, including speckle fluctuation and particle tracking. By correlating the event count with flow velocity through simulations and experiments, we first demonstrate its application in laser speckle imaging for noninvasive mapping of mouse ear vasculature and ethanol-induced hemodynamic changes. When integrated with widefield fluorescence localization microscopy and point spread function engineering, Event2Flow further enables kilohertz-rate particle tracking for rapid 3D velocity quantification in transcranial brain imaging and snapshot flow direction estimations using event polarity. Overall, Event2Flow offers a scalable alternative to conventional high-speed imaging systems for vascular and neuroimaging applications.

neuroscience↗

bioRxiv2026

A closed-loop cell therapy engineered to autonomously secrete Activin A inhibitor protects from fibrodysplasia ossificans progressiva

Engineered cell therapies present an opportunity for endogenous, site-specific production of therapeutic agents. Here we describe a closed-loop cell therapy which secretes an inhibitor of Activin A, ActR2A-Fc, upon exposure to Activin A. We demonstrate in vivo therapeutic efficacy of this approach in a mouse model of fibrodysplasia ossificans progressiva (FOP), a morbid condition in which patients develop extensive heterotopic bony lesions in response to aberrant sensitivity to Activin A through a mutation in the type I BMP receptor ACVR1 (ACVR1 R206H). To blunt Activin A activity, we designed a transposon plasmid containing the transgene encoding ActR2A-Fc, with expression controlled by the BMP-responsive element (BRE). In cells containing the causative mutation, the BRE is pathologically activated upon exposure to Activin A. FOP-derived marrow cells modified with the BRE-ActR2AFc plasmid exhibited the desired closed-loop functionality, with increased ActR2A-Fc expression upon exposure to Activin A and reduced expression upon withdrawal of Activin A. Engineered marrow cells secreted bioactive ActR2A-Fc, and bone marrow transplantation of FOP marrow cells engineered with the BRE-ActR2AFc transposon into same-sex FOP mice resulted in absence of heterotopic bony lesions. Experiments with labeled, engineered FOP marrow cells verified trafficking of the therapeutic cells to sites at risk for FOP. These data provide proof-of-concept for the therapeutic utility of engineered cell therapy for the treatment of FOP. Significance statementIn this study, we describe our development of an autologous, closed-loop cell therapy which can migrate to sites of tissue injury and locally secreting an inhibitor of Activin A. Through our use of an Activin A-responsive promoter to drive expression of the recombinant Activin A inhibitor, this engineered cell therapy exhibits closed-loop behavior and effectively prevents heterotopic bone formation in a mouse model of fibrodysplasia ossificans progressiva (FOP). We believe that the findings in this manuscript impactful beyond FOP, and provide a blueprint for the development of marrow-derived cell therapies across the disease spectrum.

cell biology↗

bioRxiv2026

Harnessing Tumor-Specific Transcript Diversity Uncovers a Shared Neoantigen Reservoir for Pancreatic Ductal Adenocarcinoma

Pancreatic ductal adenocarcinoma (PDAC) is refractory to immunotherapy due to its immunologically cold microenvironment and the scarcity of mutation-derived neoantigens. Here, we introduce NeoAPP, a computational tool designed to systematically decode neoantigens arising from tumor-specific transcripts (TSTs) generated by transcriptional dysregulation. Multi-cohort transcriptomic profiling of 413 PDAC samples using NeoAPP reveal a median of 351 neoantigens per sample derived from 56 neoantigen-encoding TSTs (neoTSTs), surpassing mutation-derived counterparts in both abundance and patient coverage. Mechanistic analyses show that non-canonical splicing junction and transposable element activation drive neoantigen generation, while FOXA2-regulated promoter usage constitutes a potential major source of neoTSTs. Tumor-derived neoTSTs are also detected in extracellular vesicles and cancer-associated fibroblasts, implicating stromal crosstalk in immune modulation. Vaccination with neoTSTs induce CD8+ T cell responses in HLA-A*02:01/A*11:01 transgenic mice and suppressed tumor growth in syngeneic PDAC models. Collectively, this work establishes TST-derived neoantigens as a dominant and therapeutically actionable antigen reservoir in PDAC, advancing a transcriptome-guided framework for neoantigen discovery with potential to overcome immune resistance in low-mutation cancers. Abstract Figure O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=196 SRC="FIGDIR/small/705024v1_ufig1.gif" ALT="Figure 1"> View larger version (71K): org.highwire.dtl.DTLVardef@82ff31org.highwire.dtl.DTLVardef@401342org.highwire.dtl.DTLVardef@b0771corg.highwire.dtl.DTLVardef@15c03ef_HPS_FORMAT_FIGEXP M_FIG C_FIG

cancer biology↗