Biology subjects

Gu, L.

Publications and source records attributed to Gu, L..

At least 37 records · Page 2Linked to original sources

bioRxiv2025

End-to-end high-throughput single-cell proteomics via SPRINT and dual-spray LC-MS

Single-cell proteomics (SCP) enables direct measurement of protein heterogeneity but remains constrained by throughput and limited applicability to primary tissues. Here, we present an integrated workflow developed to address both challenges. We engineered SPRINT, an AI-powered bioprinting platform that prepares more than 10,000 single cells per day, over tenfold faster than existing systems, while maintaining stability and enabling identification of over 6,000 proteins from individual HeLa cells. To expand analytical capacity, we further designed a dual-spray tandem direct injection (TDI) LC system that parallelizes non-analytical steps with peptide separation, doubling MS utilization efficiency and enabling 168 label-free SCP runs per day without sensitivity loss. Together with optimized tissue-dissociation protocols, this integrated workflow enabled creation of the first mouse tissue-derived SCP atlas, profiling >1,000 single cells across six organs. These advances establish SCP as a scalable platform ready for broad biological and biomedical applications.

systems biology↗

bioRxiv2025

Pervasive splicing in a plant DNA virus

RNA splicing is considered an oddity in plant viruses; here, unexpectedly, we find it to be prevalent in the geminivirus tomato yellow leaf curl virus. Transcriptome analysis revealed eight splicing events generating novel protein isoforms, six of which were validated and two shown to depend on the plant spliceosome. Splicing impairment reduced viral accumulation and symptom severity, demonstrating that splicing contributes to infectivity, potentially by expanding the viral proteome, and suggesting that plant virus transcriptomes need to be reassessed.

plant biology↗

bioRxiv2025

Chondrolectin regulates the sublaminar localization and regenerative function of muscle satellite cells in mice

Skeletal muscle satellite cells (SCs) reside between the myofiber sarcolemma and basal lamina, where extracellular matrix (ECM) interactions are essential for their maintenance and regenerative function. Here, we identify chondrolectin (CHODL), a type I transmembrane protein with a C-type lectin domain, as a critical regulator of SC biology. Single-cell RNA-seq analysis reveals that Chodl is highly enriched in quiescent SCs but downregulated in proliferating myoblasts. Using conditional knockout models, we show that deletion of Chodl in embryonic myoblasts (ChodlMKO) or adult SCs (ChodlPKO) does not affect muscle development but markedly impairs regeneration in both young and aged mice. Chodl-deficient SCs exhibit reduced self-renewal, diminish proliferation, and impair differentiation, leading to defective myofiber repair. In silico network perturbation further predicts disruption of ECM-ligand interactions and Notch signaling, consistent with our observation that a significant fraction of SCs in ChodlPKOmice localize outside the basal lamina and undergo precocious activation. Together, these findings establish CHODL as a key determinant of SC niche localization and regenerative function, uncovering a previously unrecognized mechanism linking ECM interactions to muscle stem cell maintenance and repair.

developmental biology↗

bioRxiv2025

Paclitaxel Alleviates Pulmonary Arterial Hypertension by Modulating Macrophage M2a Polarization via the NF-κB Pathway

BackgroundPulmonary arterial hypertension (PAH) is primarily associated with vascular remodeling, in which macrophage polarization is considered to play a major role. Paclitaxel(PTX) has been shown to modulate macrophage polarization in tumors. We investigated whether PTX could alleviate PAH by altering macrophage polarization, particularly M2a macrophages. MethodsTo establish PAH, rats underwent left pneumonectomy followed by monocrotaline (MCT) injection. In vitro, THP-1 cells were differentiated into macrophages using PMA and polarized with LPS+IFN-{gamma} (M1), IL-4 (M2a), or IL-10 (M2c), followed by PTX intervention. Hemodynamic parameters (mPAP) and right ventricular hypertrophy index (RVHI) were measured. Pathological changes were assessed via HE staining. Single-cell RNA sequencing analyzed macrophage subsets in lung tissues. Macrophage polarization and NF-{kappa}B pathway activity were evaluated using immunohistochemistry, qPCR, cytokine profiling and Western blot. ResultsIn a severe PAH model induced by left pneumonectomy plus monocrotaline, pulmonary interstitial macrophages initially exhibited a predominant M1-polarized phenotype in the early stage, which transitioned to an M2a-polarized phenotype in the later stage and eventually stabilized. Low-dose PTX alleviated severe PAH by reducing perivascular macrophage infiltration. Cytological studies confirmed that PTX inhibited M2a polarization via suppression of NF-{kappa}B, thereby attenuating its proliferative effects on pulmonary arterial smooth muscle cells (PASMCs). ConclusionM2a macrophages play a crucial role in PAH progression. PTX may alleviate PAH by suppressing M2a polarization via the NF-{kappa}B pathway.

immunology↗

bioRxiv2025

Lessons from a gene knockout mouse model: no phenotypes induced by deletion of the TPR4 domain of Ttc22

The TTC22 gene encodes a protein containing seven tetratricopeptide repeats (TPRs), which mediate protein-protein interactions as chaperones. We previously reported that the level of TTC22 transcript variant 1 (TTC22v1) was downregulated in human colon adenocarcinoma (COAD) and that TTC22 upregulated m6A-mediated WTAP and SNAI1 expression via the TTC22-RPL4 interaction and subsequently promoted COAD metastasis. Thus, a commercially available C57BL/6N mouse model in which the Ttc22 exon 2&3 encoding the TPR4 (equal to the human TTC22 TPR3) domain was knocked out via CRISPR-Cas9 was used to evaluate the contribution of Ttc22 to the development of mice and COAD. To determine the status of Ttc22 expression in Ttc22 knockout mice, we prepared a rabbit polyclonal antibody against the mouse Ttc22 protein, which could bind both wild type Ttc22 and TPR4-deleted Ttc22 proteins overexpressed in HEK293T cells, as determined by Western blot analysis. Ttc22 proteins were detected in colon tissue samples from wild-type mice and Ttc22 hemi-knockout (Ttc22 -/+) mice but not in those from fully Ttc22 knockout (Ttc22-/-) mice. Unfortunately, the long-term observation results demonstrated that Ttc22 knockout (KO, including Ttc22-/+ or Ttc22-/-) did not affect the body weight, development, fertility, or spontaneous tumor incidence of male or female mice. No differences in the incidence of AOM/DSS-induced COAD were observed between these mouse groups, although Ttc22 deletion partially resulted in the upregulation of genes related to the host adaptive response to inflammation in the colon mucosa. In conclusion, no phenotypes were induced by Ttc22 inactivation in C57BL/6N mice. HighlightsO_LIKnockout of Ttc22 exons 2 and 3 completely disrupted gene expression. C_LIO_LIKnockout of Ttc22 does not affect the development of C57BL mice. C_LIO_LIKnockout of Ttc22 does not affect the induction of mouse colon cancer by AOM/DSS. C_LI

molecular biology↗

bioRxiv2025

Intracellular Delivery of Bone Nanoparticles to Mitigate Irradiation-Induced Damage in Bone Marrow Mesenchymal Stem Cells

Ionizing radiation (IR)-induced bone damage presents a major clinical challenge by impairing bone marrow function and disrupting normal bone remodeling. Bone regeneration depends on bone marrow-derived mesenchymal stem cells (BMSCs), which are highly sensitive to IR that causes DNA damage, oxidative stress, apoptosis, and a shift from osteogenesis to adipogenesis, ultimately leading to bone loss and impaired healing. This study evaluated the therapeutic potential of intracellularly delivered bone-derived nanoparticles (BPs) in mitigating IR-induced BMSCs damage. We found that IR exposure caused significant BMSCs dysfunction, including reduced proliferation, increased apoptosis, persistent DNA damage, and a shift toward adipogenic differentiation. Treatment with BPs led to efficient intracellular uptake, improved cell morphology, enhanced proliferation, reduced apoptosis, and preservation of balanced differentiation capacity. Transcriptomic analysis via RNA sequencing revealed that BPs restored key molecular pathways disrupted by IR, particularly those involved in cell cycle regulation, extracellular matrix (ECM) remodeling, and apoptosis. By reversing these transcriptional impairments, BPs supported genomic stability and the regenerat ive function of BMSCs. Overall, these findings suggest that BPs effectively counteract IR-induced cellular damage and enhance the regenerative capacity of BMSCs, offering a promising therapeutic strategy for radiation -induced skeletal injuries.

bioengineering↗

bioRxiv2025

Locus Coeruleus to Medial Prefrontal Cortex Noradrenergic Neural Circuit Modulates States of Consciousness during Sevoflurane Anesthesia in Mice

How exactly does general anesthesia achieve its effects? It is so widely used in surgeries and medical treatments to enhance comfort for nearly one hundred years, yet its precise mechanisms underlying the loss and recovery of consciousness still remain unclear. Utilizing a variety of research methods-pharmacological, optogenetic, chemogenetic, fiber photometry, and gene knockdown approaches-our study has shed light on the significant modulatory function of locus coeruleus noradrenergic neurons during the transition from sevoflurane anesthesia to awakening. Furthermore, the activation of the LC-mPFC circuit has been found to have a substantial arousal effect, with 1-AR playing a crucial role in this process. Additionally, GABAA-R has been identified as the key binding site for sevoflurane within the locus coeruleus. These findings collectively offer novel insights into the neural network mechanisms underlying general anesthesia, advancing our understanding of this complex medical phenomenon.

neuroscience↗

bioRxiv2025

Genetic architecture of the S-locus supergene revealed in a tetraploid distylous species

SummaryO_LIHeterostyly is a polymorphic floral adaptation controlled by supergenes and maintained in populations by disassortative mating. The molecular basis of distyly has been investigated in several unrelated families. Previous studies have been limited to diploid species and have not included Rubiaceae, which has the highest number of heterostylous species. C_LIO_LIHere, we investigate the genetic architecture of tetraploid Schizomussaenda henryi (Rubiaceae) to identify candidate style-length genes, evidence for hemizygosity and the potential role of gene duplication in the evolution of the S-locus. Chromosome-level genome assemblies and transcriptomic approaches identified the S-locus region comprised of four hemizygous genes. C_LIO_LIThe candidate gene SchzAUX22 may regulate style length and filament growth by acting in the auxin signaling pathway. Comparative studies of the two sub-genomes of S. henryi indicated strong similarities and no significant sub-genome dominance, as expected from autotetraploidy. Evidence from haplotype-resolved assemblies of a short-styled plant indicated that it possessed the ssSS genotype, consistent with autotetraploidy, which was estimated to have originated [~]3.6 Mya. Analysis of Ks values between S-locus genes and their paralogs indicated that the S-locus likely originated through stepwise duplication. C_LIO_LIOur study provides comprehensive genomic analysis of distyly in a polyploid and demonstrates that despite whole genome doubling the S-locus supergene remains intact and functional as an outbreeding mechanism. Our results contrast with many other heterostylous lineages where polyploidy is associated with breakdown of the polymorphism and transitions to self-fertilization. C_LI

plant biology↗

bioRxiv2025

Systematic Identification of Microtubule Inner Proteins Reveals JPT2 as a Key Regulator of Lumen Microenvironment and Drug Sensitivity

Microtubules are primarily studied for the interactions of proteins that bind to their outer surfaces and ends, while the regulatory mechanisms within the microtubule lumen, particularly in singlet microtubules critical for essential cellular processes, remain largely unexplored. Our study provides the first systematic identification of key regulatory proteins within the single microtubule lumen. Using proximity-dependent biotin identification (Bio-ID) coupled with mass spectrometry, we identified candidate microtubule inner proteins (MIPs), including Jupiter microtubule-associated homolog 2 (JPT2). JPT2 binds directly to microtubules and specifically localizes within the lumen, where it modulates the luminal environment by inhibiting acetylase MEC17 and independently affects the binding and efficacy of Paclitaxel. Furthermore, our screening identified additional MIPs that influence cellular sensitivity to Paclitaxel, indicating a link between luminal regulation and drug responsiveness. These discoveries reveal JPT2s critical role in singlet microtubule regulation and suggest new therapeutic targets for enhancing cancer drug sensitivity.

cell biology↗

bioRxiv2024

Disordered glass nanowire substrates produce in vivo-like astrocyte morphology revealed by optical diffraction tomography

Astrocytes, integral components of the central nervous system (CNS), fulfill crucial roles such as maintaining ion homeostasis, providing neuroprotection, and contributing to the blood-brain barrier. Their distinctive, star-like morphology is essential to these functions, and abnormalities in astrocyte structure are linked to numerous neurological disorders. However, our understanding of astrocyte morphology, particularly in vivo, remains limited. Traditional imaging methods, such as fluorescence microscopy, introduce challenges like restricting continuous observation and comprehensive morphological analysis. In this study, we present a novel approach utilizing optical diffraction tomography (ODT), an advanced imaging technique that generates 3D refractive index profiles, to image and quantify detailed astrocyte morphology. We demonstrate, for the first time, the application of ODT to image samples through and on disordered glass nanowire (NW) substrates, overcoming the typical challenges posed by nanostructures, which can disrupt phase reconstruction. Crucially, we show that disordered glass nanowire (NW) substrates can induce in vivo-like astrocyte morphology in cultured rat cortical astrocytes. Compared to traditional glass substrates, astrocytes grown on disordered glass NWs substrates exhibited enhanced process branching and greater total arbor length--features typically observed in their natural, in vivo state, a state of advanced maturation. This finding underscores the significant influence of substrate topography on astrocyte structure and highlights the unique potential of nanostructured environments to mimic physiological conditions. By leveraging ODT, we were able to monitor astrocyte behavior on these substrates, providing unprecedented insights into their morphological dynamics. Our study pioneers the use of nanostructured substrates for reconstructing astrocyte morphology and sets the stage for further exploration of how microenvironmental cues shape astrocyte morphology and behavior.

cell biology↗

bioRxiv2024

Neural basis of collective social behavior during environmental challenge

Humans and animals have a remarkable capacity to collectively coordinate their behavior to respond to environmental challenges. However, the underlying neurobiology remains poorly understood. Here, we found that groups of mice self-organize into huddles at cold ambient temperature during the thermal challenge assay. We found that mice make active (self-initiated) and passive (partner-initiated) decisions to enter or exit a huddle. Using microendoscopic calcium imaging, we found that active and passive decisions are encoded distinctly within the dorsomedial prefrontal cortex (dmPFC). Silencing dmPFC activity in some mice reduced their active decision-making, but also induced a compensatory increase in active decisions by non-manipulated partners, conserving the groups overall huddle time. These findings reveal how collective behavior is implemented in neurobiological mechanisms to meet homeostatic needs during environmental challenges.

neuroscience↗

bioRxiv2024

Biofabrication of Small Vascular Graft with Acellular Human Amniotic Membrane: A Proof-of-Concept Study in Pig

Synthetic vascular grafts, such as expanded polytetrafluoroethylene (ePTFE), are commonly used for large vessel surgeries [internal diameter (ID) [≥] 10 mm] but present significant challenges in medium to small vessels (ID < 10 mm) due to increased risks of thrombosis, stenosis, and infection. In this study, we developed a small-diameter vascular graft using decellularized human amniotic membrane (DAM graft) (ID = 6 mm) and transplanted it into porcine carotid arteries, comparing it with ePTFE grafts to assess inflammation, biocompatibility, patency, and overall function. One-week post-implantation, ultrasound imaging confirmed blood patency in both graft types. However, after one-month, gross examination revealed pronounced neointimal hyperplasia in ePTFE grafts, while DAM grafts maintained open lumens without signs of stenosis or thrombosis. Histological analysis showed extensive fibrous tissue formation in ePTFE grafts, resulting in luminal narrowing, whereas DAM grafts displayed sustained lumen patency and vascular integration. Immunofluorescence confirmed reduced inflammation and improved tissue organization in DAM grafts, characterized by lower macrophage infiltration and better cellular architecture. These findings suggest that DAM grafts offer superior biocompatibility and significantly lower risks of neointimal hyperplasia, making them a promising alternative for small-diameter vascular surgeries compared to ePTFE grafts.

bioengineering↗

bioRxiv2024

gilgamesh, Drosophila casein kinase 1g, is required for myosin-dependent junction strengthening and epithelial folding

Adherens junctions, which serve as the primary physical link between cells, undergo remodeling in response to tension forces to maintain tissue integrity and promote tissue shape changes. However, the in vivo mechanisms driving this process remain poorly understood. Here, we identified Gilgamesh (Gish), the conserved fly homolog of casein kinase 1g as essential for myosin-dependent junction strengthening and tissue folding during apical constriction of Drosophila mesoderm. We show that Gish is recruited to spot adherens junctions in a contractile myosin-dependent manner. During apical constriction, Gish is required for junction strengthening by promoting growth and merging of small junction puncta, as well as stabilizing junction puncta at cell edges. The junction defects in Gish-depleted mesoderm result in breakage of the tissue-scale apical actomyosin network during apical constriction, and ultimately failure in mesoderm infolding. Our data show that Gish is a mechanosensitive kinase required for the integrity of adherens junctions during apical constriction.

developmental biology↗

bioRxiv2024

Design of linked-domain protein inhibitors of UBE2D as tools to study cellular ubiquitination

Ubiquitin (Ub) is a post-translational modification that largely controls proteostasis through mechanisms spanning transcription, translation, and notably, protein degradation. Ub conjugation occurs through a hierarchical cascade of three enzyme classes (E1, E2, and E3s) involving >1000 proteins that regulate the ubiquitination of proteins. The E2 Ub-conjugating enzymes are the midpoint, yet their cellular roles remain under-characterized, partly due to a lack of inhibitors. For example, the cellular roles of the promiscuous E2 UBE2D/UBCH5 are not well described. Here, we develop a highly selective, multivalent, engineered protein inhibitor for the UBE2D family that simultaneously targets the RING- and backside-binding sites. In HeLa cells, these inhibitors phenocopy knockdown of UBE2D by reducing the IC50 to cisplatin and whole-cell proteomics reveal an increased abundance of [~]20% of the identified proteins, consistent with reduced Ub degradation and proteotoxic stress. These precision tools will enable new studies probing UBE2Ds central role in proteome management.

biochemistry↗

bioRxiv2024

Uncovering Astrocyte Morphological Dynamics Using Optical Diffraction Tomography and Shape-based Trajectory Inference

Astrocytes, integral components of the central nervous system, are increasingly recognized for their multifaceted roles beyond mere support cells. Despite their acknowledged importance, understanding the intricacies of astrocyte morphology and dynamics remains limited. Our study marks the first exploration of astrocytes using optical diffraction tomography (ODT), aiming to establish a solid foundation for their detailed characterization. It offers valuable insights into the morphological changes in postnatal rat cortical astrocytes over a 7-day in vitro period in a label-free manner. Through comprehensive analysis of 3D refractive index maps and shape characterization techniques, we elucidate the developmental trajectory and dynamic morphological transformations of astrocytes in culture. Specifically, our observations revealed increased area and transition to larger, flattened shapes, and alterations in cell volume and density, indicating shifts in cellular composition. Furthermore, by employing unsupervised clustering and pseudotime trajectory analysis, we tracked the morphological evolution of astrocytes from highly directional to evenly spread shapes. These results emphasize the dynamic nature of astrocytes. In addition, this analysis marks the first use of trajectory inference based solely on morphology for neural cell types. Future studies could employ ODT to examine the morphological dynamics and interactions of various neural cell types on other types of substrates.

cell biology↗

bioRxiv2024

PRMT7 mediated PTEN activation promotes bone formation in female mice

Although the epigenetic mechanisms underlying bone formation are recognized, their specific roles and regulatory pathways remain largely unexplored. In this study, we unveil PRMT7 as a novel epigenetic modulator of MSCs osteogenic commitment. The conditional knockout of Prmt7 in mice reveals significantly impaired osteogenesis and bone regeneration exclusively in females, affecting both long bones and craniofacial structures, with no discernible impact in males. Our findings demonstrate that PRMT7 orchestrates osteogenic differentiation through a methyltransferase-dependent manner. Mechanistically, PRMT7 modulates MSCs osteogenic differentiation through the activation of PTEN. Specifically, PRMT7 augments PTEN transcription by increasing H3R2me1 levels at the PTEN promoter. Furthermore, PRMT7 interacts with the PTEN protein, and its deficiency leads to the ubiquitination and subsequent degradation of nuclear PTEN, revealing an unprecedented pathway. Crucially, PTEN overexpression ameliorates the osteogenic deficits observed in Prmt7-deficient mice. Our research positions PRMT7 as a potential therapeutic target to enhance bone formation and offers novel molecular insights into the PRMT7-PTEN regulatory axis, underscoring its significance in bone biology and regenerative medicine. Subject Categories Developmental Biology, Musculoskeletal System, Epigenetics, Post-translational Modifications

developmental biology↗

bioRxiv2024

Modulation Of SUDEP By Central Serotonergic Cooperating with Noradrenergic Circuits: A Synergistic-Dependent Manner

Sudden unexpected death in epilepsy (SUDEP) is the leading cause of death in refractory epilepsy patients. Despite previous accumulating evidence has shown that seizure-induced respiratory arrest (S-IRA) may play the main contributor to SUDEP as an initiating event preeminent cause of mortality, the specific underlying mechanism of action remains unclear. Based on our previous work, serotonin (5-HT) signaling in the dorsal raphe nucleus (DRN) is strongly implicated in S-IRA in animal models, including the DBA/1 mice, on the meanwhile, norepinephrine (NE) neurons of the locus coeruleus (LC) also plays a vital role in regulating respiratory function on its own. Superficially, monoaminergic neuron, as important neurotransmitters in the central nervous system, have similar modes of action in the maintenance of nervous system balance, and each of them has a regulatory effect on SUDEP. However, it remains to be investigated whether monoaminergic neuron family (NE and 5-HT) are related in the mechanism of regulating SUDEP, what is even more curious is whether the two are intrinsically linked. Thus, we hypothesize neural mechanism of central noradrenergic and serotonergic circuits in modulating SUDEP in a synergistic-dependent manner, this endeavor will culminate in a significant breakthrough in elucidating the precise mechanism of action underlying SUDEP. In our study, we will use chemogenetics, optogenetics, calcium signal recording, and bidirectional tracing to explore the internal mechanism of DR-LC regulating the occurrence of SUDEP, and by specifically injecting 5-HT2AR antagonist Ketanserin (KET) and/or NE-1R antagonist Prazosin into the pre-Botzinger complex (PBC), it was finally elucidate that the DR-LC-PBC network can effectively reduce the incidence of SIRA. We firstly proposed a powerful target for exploring the reduction of the incidence of SUDEP, which has great clinical translation potential.

neuroscience↗

bioRxiv2024

Integrated Analysis of Single-Cell and Bulk RNA-Seq Data reveals that Ferroptosis-Related Genes Mediated the Tumor Microenvironment predicts Prognosis, and guides Drug Selection in Triple-Negative Breast Cancer

BackgroundTriple-negative breast cancer (TNBC) is aggressive, lacking methods to predict recurrence and drug sensitivity. Ferroptotic heterogeneity varies in TNBC subtypes. However, the tumor microenvironment (TME) mediated by ferroptosis genes is unclear. Our study aims to integrate single-cell and bulk RNA sequencing (RNA-seq) data to reveal the ferroptosis-mediated TME in TNBC, predicting prognosis and guiding treatment. MethodsThe single-cell and bulk RNA-seq data of TNBC were sourced from the Gene Expression Omnibus (GEO) database. Using these data, a machine learning algorithm was employed to integrate and analyze the characteristics of the TME mediated by ferroptosis-related genes in TNBC. Prediction models for TNBC survival prognosis and drug treatment response were established and then validated in an independent set. ResultsAt the individual cell level, T cells were categorized into three distinct subpopulations, and local macrophages into two subpopulations. The infiltration degree of these different cell subpopulations was closely associated with prognosis and treatment outcomes. Based on this, the risk score model we developed effectively predicted recurrence-free survival in TNBC patients, with independently validated pooled predicted 3-, 4-, and 5-year Area Under the Curves (AUCs) of 0.65, 0.67, and 0.71, respectively. Additionally, we found that patients in the high-risk group may be more responsive to 27 drugs. ConclusionsWe have uncovered the tumor immune cell clusters in TNBC mediated by ferroptosis. A risk score model was constructed to identify high-risk TNBC patients, which can assist physicians in disease monitoring and precision therapy. The genes identified hold significant potential as therapeutic targets for TNBC patients. FundingThis project is funded by the National Natural Science Foundation of China (81974268, 82472000, 82304151), the Talent Incentive Program of Cancer Hospital Chinese, Academy of Medical Sciences (801032247), the Cooperation Fund of CHCAMS (CFA202202023), and the open project of Beijing Key Laboratory of Tumor Invasion and Metastasis Mechanism, Capital Medical University(2023ZLKF03). Impact StatementIntegrating single-cell and bulk RNA-seq data elucidates the role of ferroptosis in TNBC, offering a prognostic model and personalized therapeutic insights.

cancer biology↗