Bio

Claudia Del Toro Runzer is a postdoctoral scholar at Stanford University specializing in gene therapy and regenerative medicine. Her current research focuses on developing gene editing strategies for inherited disorders, including GNE myopathy and Gaucher disease. She works on advancing precision gene engineering approaches in human hematopoietic stem and progenitor cells and other clinically relevant cell types, with the goal of enabling safe and durable therapeutic correction.

Dr. Del Toro Runzer earned her PhD in Tissue Engineering from the MERLN Institute for Technology-Inspired Regenerative Medicine at Maastricht University. Her doctoral research focused on chemically modified mRNA therapeutics for bone regeneration, where she investigated molecular design, intracellular trafficking, and biomaterial-assisted delivery systems to enhance protein expression and osteogenic outcomes. Her work resulted in multiple first-author publications in leading journals, including Advanced Functional Materials, Bone Research, Materials Today, and Molecular Therapy: Nucleic Acids.

Prior to her PhD, she completed an M.Sc. in Regenerative Biology and Medicine at Technische Universität Dresden and a B.Sc. in Biotechnology Engineering at Instituto Tecnológico de Monterrey. Her international training spans Germany, the Netherlands, Mexico, and the United States, with research experience in organoid systems, tissue regeneration, biomaterials engineering, and microphysiological platforms.

Institute Affiliations

Stanford Advisors

Contact

  • Academic
    claudtr@stanford.edu
    University - Scholar Department: Pediatrics Position: Postdoctoral Scholar

Additional Info

All Publications

  • Biologics for bone regeneration: advances in cell, protein, gene, and mRNA therapies BONE RESEARCH Runzer, C., Balmayor, E. R., van Griensven, M. 2026; 14 (1): 5

    Abstract

    Bone fractures represent a significant global healthcare burden. Although fractures typically heal on their own, some fail to regenerate properly, leading to nonunion, a condition that causes prolonged disability, morbidity, and mortality. The challenge of treating nonunion fractures is further complicated in patients with underlying bone disorders where systemic and local factors impair bone healing. Traditional treatment approaches, including autografts, allografts, xenografts, and synthetic biomaterials, face limitations such as donor site pain, immune rejection, and insufficient mechanical strength, underscoring the need for alternative strategies. Biologic therapies have emerged as promising tools to enhance bone regeneration by leveraging the body's natural healing processes. This review explores the critical role of conventional and emerging biologics in fracture healing. We categorize biologic therapies into protein-based treatments, gene and transcript therapies, small molecules, peptides, and cell-based therapies, highlighting their mechanisms of action, advantages, and clinical relevance. Finally, we examine the potential applications of biologics in treating fractures associated with bone disorders such as osteoporosis, osteogenesis imperfecta, rickets, osteomalacia, Paget's disease, and bone tumors. By integrating biologic therapies with existing biomaterial-based strategies, these innovative approaches have the potential to transform clinical management and improve outcomes for patients with difficult-to-heal fractures.

    View details for DOI 10.1038/s41413-025-00487-0

    View details for Web of Science ID 001658614100003

    View details for PubMedID 41521187

    View details for PubMedCentralID PMC12791149

  • Engineering bone tissue with mRNA: from molecular design and delivery to clinical applications MATERIALS TODAY Runzer, C., Van Griensven, M., Balmayor, E. 2025; 91: 124-147

    View details for DOI 10.1016/j.mattod.2025.11.002

    View details for Web of Science ID 001637326100001

  • Synergistic Osteogenesis After Co-Administration of cmRNAs Encoding BMP-2 and BMP-7 Utilizing a Transcript-Activated Matrix ADVANCED FUNCTIONAL MATERIALS Del Toro Runzer, C., Sadowska, J. M., Roumans, N., Plank, C., Evans, C. H., O'Brien, F. J., van Griensven, M., Balmayor, E. R. 2026; 36 (10)

    View details for DOI 10.1002/adfm.202508631

    View details for Web of Science ID 001566389800001

  • Cellular uptake of modified mRNA occurs via caveolae-mediated endocytosis, yielding high protein expression in slow-dividing cells. Molecular therapy. Nucleic acids Del Toro Runzer, C., Anand, S., Mota, C., Moroni, L., Plank, C., van Griensven, M., Balmayor, E. R. 2023; 32: 960-979

    Abstract

    Nucleic acids have clear clinical potential for gene therapy. Plasmid DNA (pDNA) was the first nucleic acid to be pursued as a therapeutic molecule. Recently, mRNA came into play as it offers improved safety and affordability. In this study, we investigated the uptake mechanisms and efficiencies of genetic material by cells. We focused on three main variables (1) the nucleic acid (pDNA, or chemically modified mRNA), (2) the delivery vector (Lipofectamine 3000 or 3DFect), and (3) human primary cells (mesenchymal stem cells, dermal fibroblasts, and osteoblasts). In addition, transfections were studied in a 3D environment using electrospun scaffolds. Cellular internalization and intracellular trafficking were assessed by using enhancers or inhibitors of endocytosis and endosomal escape. The polymeric vector TransIT-X2 was included for comparison purposes. While lipoplexes utilized several entry routes, uptake via caveolae served as the main route for gene delivery. pDNA yielded higher expression levels in fast-dividing fibroblasts, whereas, in slow-dividing osteoblasts, cmRNA was responsible for high protein production. In the case of mesenchymal stem cells, which presented an intermediate doubling time, the combination vector/nucleic acid seemed more relevant than the nucleic acid per se. In all cases, protein expression was higher when the cells were seeded on 3D scaffolds.

    View details for DOI 10.1016/j.omtn.2023.05.019

    View details for PubMedID 37305166

    View details for PubMedCentralID PMC10250585

  • Inside the cell: Approaches to evaluating mRNA internalization and trafficking. Methods (San Diego, Calif.) Del Toro Runzer, C., Plank, C., van Griensven, M., Balmayor, E. R. 2025; 241: 173-183

    Abstract

    With the growing prominence of mRNA-based therapeutics and vaccines, accurately assessing the cellular uptake of mRNA complexes is a critical first step in evaluating both the efficiency of delivery systems and their downstream therapeutic potential. This is especially important when working with novel mRNA constructs, comparing different delivery vectors, or targeting diverse cell types. In this study, we present a suite of methods to quantify and visualize mRNA internalization following transfection of three types of human primary cells: mesenchymal stromal cells, fibroblasts, and osteoblasts. We highlight the utility of fluorescent probes for both qualitative and quantitative assessment of mRNA uptake and intracellular trafficking. To dissect the pathways involved in uptake, we employed three distinct endocytic inhibitors-chlorpromazine, wortmannin, and genistein-each targeting specific endocytic mechanisms. Additionally, we provide protocols for the lipid-based transfection agents Lipofectamine 3000 and 3DFect, which can be adapted for use with similar vectors. Key methodologies such as flow cytometry and correlative light and electron microscopy, known as CLEM, are described in detail for their effectiveness in analyzing mRNA internalization. A deeper understanding of the internalization and intracellular fate of mRNA is essential for the advancement of more efficient and safer mRNA-based delivery platforms.

    View details for DOI 10.1016/j.ymeth.2025.06.006

    View details for PubMedID 40513751

  • Acoustically Responsive Nanofibrous Scaffolds with 3D Hierarchy for Tympanic Membrane Regeneration SMALL STRUCTURES Anand, S., Del Toro Runzer, C., Rosado Balmayor, E., van Griensven, M., Moroni, L., Mota, C. 2025

    View details for DOI 10.1002/sstr.202500155

    View details for Web of Science ID 001531650200001

  • Implementing BMP-7 Chemically Modified RNA for Bone Regeneration with 3D Printable Hyaluronic Acid-Collagen Granular Gels. Advanced healthcare materials van der Heide, D., Del Toro Runzer, C., Della Bella, E., Plank, C., van Griensven, M., Balmayor, E. R., Stoddart, M. J., D'Este, M. 2025; 14 (19): e2405047

    Abstract

    Chemically modified RNA (cmRNA) is emerging as a more effective alternative to protein delivery and DNA-based gene therapy. To implement this technology for bone regeneration, a suitable biomaterial functioning as scaffold and delivery system is necessary. This study introduces a 3D printable granular hydrogel consisting of hyaluronic acid and collagen (THA-Col) for the delivery of bone morphogenetic protein (BMP)-7 cmRNA as activated matrix to promote bone healing. Granular hydrogels are produced by mechanically fragmenting bulk THA-Col gels. Resulting microgels are 3D printable and are further investigated in comparison to bulk THA-Col gels for BMP-7 cmRNA transfection efficiency, cytotoxicity, and osteogenic differentiation of human mesenchymal stromal cells (hMSCs). Microgels showed higher cell viability than bulk gels, while both bulk and microgels could support transfection with BMP-7. During in vitro osteogenic differentiation, hMSCs on microgels showed higher production of alkaline phosphatase (ALP) compared to bulk gels. The combination of microgels loaded with BMP-7 cmRNA introduced in this work holds significant potential toward the development of patient-specific bone graft substitutes to replace autologous bone grafting and protein delivery.

    View details for DOI 10.1002/adhm.202405047

    View details for PubMedID 40465277

    View details for PubMedCentralID PMC12304813

  • Modeling inducible neuropathologies of the retina with differential phenotypes in organoids. Frontiers in cellular neuroscience Völkner, M., Wagner, F., Kurth, T., Sykes, A. M., Del Toro Runzer, C., Ebner, L. J., Kavak, C., Alexaki, V. I., Cimalla, P., Mehner, M., Koch, E., Karl, M. O. 2023; 17: 1106287

    Abstract

    Neurodegenerative diseases remain incompletely understood and therapies are needed. Stem cell-derived organoid models facilitate fundamental and translational medicine research. However, to which extent differential neuronal and glial pathologic processes can be reproduced in current systems is still unclear. Here, we tested 16 different chemical, physical, and cell functional manipulations in mouse retina organoids to further explore this. Some of the treatments induce differential phenotypes, indicating that organoids are competent to reproduce distinct pathologic processes. Notably, mouse retina organoids even reproduce a complex pathology phenotype with combined photoreceptor neurodegeneration and glial pathologies upon combined (not single) application of HBEGF and TNF, two factors previously associated with neurodegenerative diseases. Pharmacological inhibitors for MAPK signaling completely prevent photoreceptor and glial pathologies, while inhibitors for Rho/ROCK, NFkB, and CDK4 differentially affect them. In conclusion, mouse retina organoids facilitate reproduction of distinct and complex pathologies, mechanistic access, insights for further organoid optimization, and modeling of differential phenotypes for future applications in fundamental and translational medicine research.

    View details for DOI 10.3389/fncel.2023.1106287

    View details for PubMedID 37213216

    View details for PubMedCentralID PMC10196395

  • HBEGF-TNF induce a complex outer retinal pathology with photoreceptor cell extrusion in human organoids. Nature communications Völkner, M., Wagner, F., Steinheuer, L. M., Carido, M., Kurth, T., Yazbeck, A., Schor, J., Wieneke, S., Ebner, L. J., Del Toro Runzer, C., Taborsky, D., Zoschke, K., Vogt, M., Canzler, S., Hermann, A., Khattak, S., Hackermüller, J., Karl, M. O. 2022; 13 (1): 6183

    Abstract

    Human organoids could facilitate research of complex and currently incurable neuropathologies, such as age-related macular degeneration (AMD) which causes blindness. Here, we establish a human retinal organoid system reproducing several parameters of the human retina, including some within the macula, to model a complex combination of photoreceptor and glial pathologies. We show that combined application of TNF and HBEGF, factors associated with neuropathologies, is sufficient to induce photoreceptor degeneration, glial pathologies, dyslamination, and scar formation: These develop simultaneously and progressively as one complex phenotype. Histologic, transcriptome, live-imaging, and mechanistic studies reveal a previously unknown pathomechanism: Photoreceptor neurodegeneration via cell extrusion. This could be relevant for aging, AMD, and some inherited diseases. Pharmacological inhibitors of the mechanosensor PIEZO1, MAPK, and actomyosin each avert pathogenesis; a PIEZO1 activator induces photoreceptor extrusion. Our model offers mechanistic insights, hypotheses for neuropathologies, and it could be used to develop therapies to prevent vision loss or to regenerate the retina in patients suffering from AMD and other diseases.

    View details for DOI 10.1038/s41467-022-33848-y

    View details for PubMedID 36261438

    View details for PubMedCentralID PMC9581928

  • Thymidylate synthase polymorphism in Mexican patients with colon cancer treated with 5-fluorouracil. Journal of B.U.ON. : official journal of the Balkan Union of Oncology Patricia Rios-Ibarra, C., Janeth Rodriguez-Silva, C., Alonso Lopez-Chuken, Y., Ortiz-Lopez, R., Fernandez-Castillo, E., Beatriz Del Toro Runzer, C., Paul Armenta-Perez, V., Flores-Gutierrez, J. P., Quintanilla-Guzman, A., Salinas-Santander, M., Gonzalez-Guerrero, J. F., Bosques-Padilla, F., Santos, A., Guadalupe Martinez-Rodriguez, H. 2016; 21 (4): 935-940

    Abstract

    We analyzed the genotype and allele frequency of variable number tandem repeats (VNTR)-thymidylate synthase (TS) and its relationship with the disease evolution in colon cancer patients.We selected 24 paraffin-embedded colon cancer tissue samples from Mexican patients who received a 5-fluorouracil (5-FU)-based chemotherapy regimen. Tumor tissue was digested with proteinase K and genomic DNA was isolated by the standard method with phenol-chloroform extraction. Polymerase chain reaction (PCR) was performed for TS genotyping of VNTR and the results were evaluated directly in a stained agarose gel.The allele frequency of 2 repeats (2R) was greater (0.66) than 3R (0.34) in metastatic colon cancer (x2=10.24; p=0.001)) however, no difference in allelic distribution between 2R (0.54) and 3R (0.46) in non metastatic patients was observed (x2=0.640; p=0.424).Our results suggest that Mexican patients with colon cancer present differences in the allelic distribution, the 2R allele being the most frequent.

    View details for PubMedID 27685916

https://orcid.org/0000-0003-4284-7368