About

David Beebe is the John D. MacArthur Professor and Claude Bernard Professor of Biomedical Engineering at the University of Wisconsin–Madison. His research aims for a holistic approach to understanding cell behavior by integrating in vitro cellular scale engineering to recapitulate important in vivo microenvironmental characteristics. This approach provides biological insights, aids in diagnosis and treatment, and enhances discovery. His work includes exploring the role of microfluidics in biomedical research and developing personalized in vitro cancer models to predict therapeutic responses. Additionally, he has contributed to understanding innate immune cell responses to host-parasite interactions within human intestinal microphysiological systems.

Research topics

• Computer Science
• Materials science
• Biology
• Nanotechnology
• Cancer research
• Cell biology
• Immunology
• Telecommunications
• Environmental science
• Microbiology
• Medicine
• Ecology
• Chemistry
• Engineering
• Pathology
• Biochemistry
• Computational biology
• Petroleum engineering

Selected publications

• Multiplexed Luminal Tissue Constructs with Reconfigurable Barriers for Dynamic Modeling of Multi‐Tissue Interactions (Adv. Mater. Technol. 5/2026)

  Advanced Materials Technologies · 2026-03-01

  articleSenior author

  Luminal Tissue Constructs This cover image illustrates a microfluidic platform generating arrays of lumen-patterned 3D tissues in extracellular matrix hydrogels within a standard well-plate footprint. An inert-oil-based, reconfigurable barrier compartmentalizes adjacent chambers or is replaced by culture medium to bridge them, enabling independently controlled, time-dependent multi-tissue studies for advanced in vitro disease modeling and drug discovery. More details can be found in the Research Article by Mouhita Humayun, Sheena C. Kerr, Adeel Ahmed, David J. Beebe, and co-workers (10.1002/admt.202500429).

  PublisherDOI

• CXCL13-CXCR5 Signaling in CD8⁺ T Cell Recruitment and Lymphoid Immune Organization in Clear Cell Renal Cell Carcinoma

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-05-07

  articleOpen access

  ABSTRACT Clear cell renal cell carcinoma (ccRCC) exhibits heterogeneity in immune infiltration and clinical outcomes, but the mechanisms governing recruitment and organization of tumor-reactive CD8⁺ T cells remain incompletely defined. We investigated the role of the CXCL13–CXCR5 axis in shaping CD8⁺ T cell recruitment, differentiation, and immune organization in high-risk, non-metastatic ccRCC. Human tumor, plasma, and matched adjacent kidney specimens were analyzed using ELISA, quantitative PCR, migration assays, multiplex immunofluorescence, single-cell RNA sequencing, spatial transcriptomics, and a syngeneic mouse model. CXCL13 was among the most upregulated chemokines in ccRCC relative to matched normal kidney and was embedded within a CD8⁺ T cell-associated inflammatory transcriptional program. In transwell and microphysiological system (MPS) assays, CXCL13 promoted CD8⁺ T cell migration, enriched CXCR5⁺ cells among migrating CD8⁺ T cells and showed reduced migration after CXCL13 or CXCR5 blockade. Single-cell analyses identified CXCR5 expression within stem-like CD8⁺ T cell states associated with TCF7 and IL7R , whereas CXCL13 associated with later cytotoxic/exhausted states along a continuous differentiation landscape. Spatial transcriptomics demonstrated that stem-like CD8⁺ T cells localized within structured lymphoid aggregates enriched for B cells, coordinated CXCL13/CXCR5 expression, and signaling programs. In vivo , tumor-derived CXCL13 suppressed tumor growth, increased intratumoral CD8⁺ T cell infiltration, and enriched CXCR5⁺TCF1⁺CD8⁺ stem-like T cells. In human tumors, higher CXCL13 expression correlated with increased CXCR5⁺CD8⁺ T cell infiltration and improved recurrence-free survival. These findings identify CXCL13 as a regulator of immune recruitment and niche organization and support the CXCL13–CXCR5 axis as a biomarker and possible therapeutic target in ccRCC.

  PublisherDOI

• Abstract A042: Modeling CAF-mediated therapy resistance in 3D prostate cancer systems using STACKs and LumeNEXT

  Cancer Research · 2026-01-20

  article

  Abstract Background: Prostate cancer (PCa) is the second leading cause of cancer-related death among men, primarily driven by hormonal mechanisms. First-line treatments include androgen deprivation therapy and androgen receptor pathway inhibitors (ARPIs); however, resistance to these treatments often leads to castration-resistant prostate cancer. Cancer-associated fibroblasts (CAFs) within the tumor microenvironment (TME) significantly influence treatment resistance; however, their interaction with tumor cells remains poorly understood due to a lack of suitable model systems. Methods: We hypothesized that CAFs reduce the cytotoxic effects of docetaxel chemotherapy and the ARPI darolutamide. To investigate this, we established two 3D co-culture systems: STACKs and LumeNEXT allowing us to examine treatment outcomes in the context of the PCa TME. STACKs enables high-throughput assessments, while LumeNEXT recapitulates the TME architecture, including engineered blood vessel mimics to study vascular and epithelial interactions involved in metastasis. We treated androgen-sensitive (LNCaP, LAPC4) and androgen-resistant (22Rv1) tumor spheroids with 10 μM darolutamide or 20 nM docetaxel, in the presence or absence of immortalized CAFs (hPrCSC-44) or normal myofibroblasts (WPMY-1) within the STACKs system. Cytotoxicity was assessed using confocal microscopy. Ongoing work aims to enhance the model by incorporating patient-derived fibroblasts from PCa patients. We characterized primary fibroblasts through bulk RNA sequencing and histological analysis and optimized co-culture conditions before introducing primary CAFs into the LumeNEXT model. Additionally, we included new genetically engineered tumor cell lines (p53/Rb1 double knockout, wild-type, and APIPC) that represent common mutations found in PCa. To measure cell death, we calculated the ratio of Ethidium homodimer+ and Hoechst+ nucleated cells to the total number of Hoechst+ cells in spheroids (≥100 µm). Statistical analyses were conducted using a two-way ANOVA and Tukey's multiple comparisons test. Results: In the STACKs, CAFs significantly reduced docetaxel toxicity in LAPC4, LNCaP, and 22Rv1 compared to conditions without CAFs (LAPC4: p<0.001, LNCaP: p<0.001, 22Rv1: p<0.001). Similarly, CAFs decreased darolutamide toxicity in LAPC4 and LNCaP cells (both p<0.001), while as expected 22Rv1 showed no response to darolutamide. Myofibroblasts had no significant effect on treatment efficacy. In the LumeNEXT system, CAFs again diminished darolutamide and docetaxel-induced cell death in LNCaP cells compared to conditions without CAFs (Docetaxel: p<0.001, Darolutamide: p<0.001). Conclusions: Our findings indicate that CAFs can attenuate the cytotoxic effects of ARPIs and docetaxel in 3D PCa TME models, highlighting their crucial role in treatment resistance. Ongoing research will further investigate the impact of patient-derived fibroblasts and the underlying molecular mechanisms through single-cell RNA sequencing. Citation Format: Nikolett Lupsa, Erika Heninger, Kate Vietor, Shannon R. Reese, Xavier T. Hazelberg, Jacob Popp, Aaron M. LeBeau, David J. Beebe, Sheena C. Kerr, Joshua M. Lang. : Modeling CAF-mediated therapy resistance in 3D prostate cancer systems using STACKs and LumeNEXT [abstract]. In: Proceedings of the AACR Special Conference in Cancer Research: Innovations in Prostate Cancer Research and Treatment; 2026 Jan 20-22; Philadelphia PA. Philadelphia (PA): AACR; Cancer Res 2026;86(2_Suppl):Abstract nr A042.

  PublisherDOI

• Abstract A030: Lossless altered histone modification analysis system to investigate patient derived cancer organoids and circulating tumor cells from patients with prostate cancer

  Cancer Research · 2026-01-20

  article

  Abstract Introduction Aberrant histone modifications and chromatin structure alter gene expression that drive phenotypic and functional behavior of aggressive prostate cancer. Technological limitations have constrained comprehensive analyses of epigenomic alterations to less relevant immortalized cell lines and pre-clinical models, as many current epigenomic assay techniques require hundreds of thousands of cells, thus limiting interrogation of clinical samples. To facilitate rare cell epigenetic analysis in patient derived cancer organoids (PDCOs) and circulating tumor cells (CTCs) from patients with prostate cancer, we miniaturized the Cleavage Under Targets and Tagmentation (CUT&Tag) assay with an Exclusive Liquid Repellency (ELR)-enabled “Lossless Altered Histone Modification Analysis System” (LAHMAS) device. CUT&Tag was developed to investigate protein-DNA interactions with high resolution, lower background and decreased cellular input requirements relative to ChIP but performance is less reliable for low inputs, making analysis of rare cell samples difficult for cell number <5000. Methods: Organoids were grown from primary tumor samples from 3 patient undergoing prostatectomy. There were a total of 5 loci collected. These samples were digested to single cells prior to assessment in the Cut&Tag assay with an antibody to H3K27Me3 or control IgG. Each sample was paired with RNAseq to assess gene expression. Results: Performing CUT&Tag on the LAHMAS device increases the signal to for very low input samples, enabling the investigation of chromatin dynamics in rare cell sample types, including PDCOs and CTCs. We observed significantly higher FRiP scores using the microscale method compared to macroscale method (average 30.3% vs 18.2%, p<0.0001) facilitating accurate chromatin profiling of low input and rare cell samples. H3K27Me3 peaks are conserved from 3000 down to 50 nuclei in cell line models on the LAHMAS device. We are evaluated H3K27Me3 histone modifications from PDCOs grown from prostatectomy samples from 3 patiens using the LAHMAS device. We obtained high quality results from these samples, obtaining yields (LNCaP: 0.147-5.15 [median: 1.13] vs. PDCO: 0.144-5.36 [0.445]), and MACS2 FRiP scores (LNCaP: 1.79-29.91 [median: 4.91] vs. PDCO: 0.73-10.21 [5.76]) similar to cell line sample. We have also leveraged the LAHMAS device to evaluate circulating tumor cells from a patient with prostate adenocarcinoma progressing on chemotherapy. This patient demonstrated high expression of ASCL1 (0 tpm) and low expression KLK3 (16237.6 tpm) by RNAseq. Concordantly, we detected H3K27Me3 peaks at the promoter of ASCL1, consistent with the repression of transcription. Conclusions: The pairing of this LAHMAS microfluidic device with a highly sensitive CUT&Tag assay has enabled the investigation of chromatin dynamics in rare cells such as PDCOs and CTCs to evaluate the contribution of these molecular alterations in tumorigenesis and treatment resistance. Citation Format: Zachary J. Kauffman, Kevin Koesser, Kyle T. Helzer, Marina N. Sharifi, Erika Heninger, Emma E. Recchia, David Kosoff, David F. Jarrard, Shuang G. Zhao, Jamie M. Sperger, David J. Beebe, Joshua M. Lang. Lossless altered histone modification analysis system to investigate patient derived cancer organoids and circulating tumor cells from patients with prostate cancer [abstract]. In: Proceedings of the AACR Special Conference in Cancer Research: Innovations in Prostate Cancer Research and Treatment; 2026 Jan 20-22; Philadelphia PA. Philadelphia (PA): AACR; Cancer Res 2026;86(2_Suppl):Abstract nr A030.

  PublisherDOI

• Abstract A023: Differential Patterns of Immune Infiltration in the Tumor Immune Microenvironment Associate with Therapeutic Response in Primary Prostate Cancer Following Chemohormonal Therapy

  Cancer Research · 2026-01-20

  article

  Abstract Background: There is a critical need to develop novel therapeutic strategies and diagnostic tools to precisely deliver treatments to improve survival for men with prostate cancer (PCa). To support this development, improved strategies are needed to better understand heterogenous tumor microenvironments and tumor biology that associate with variable treatment responses. We hypothesized that the tumor immune microenvironment (TIME) plays a critical role in treatment resistance. In this study we aimed to evaluate TIME signatures of treatment response and resistance utilizing a novel, integrated technological tool to identify response patterns and enable precision sampling for comparative cellular and molecular analysis. Methods: 30 patients with newly-diagnosed, locally advanced, high-risk, primary PCa underwent 18F-DCFPyL PSMA PET with multiparametric MRI (mpMRI) imaging on a dedicated PET/MRI scanner followed by 3 cycles of chemohormonal therapy (NCT03358563). Repeat PSMA PET/MRI was performed prior to prostatectomy and scans were interpreted by an experienced radiologist and nuclear medicine physician as complete response (CR), partial response (PR), no response (NR) or normal tissue. MRI scans were used to print a 3D mold of the prostate to allow PET and MRI directed mapping and microdissection of regions of interest from the resected prostate with slice-by-slice and lesion-to-lesion correlation. Cellular infiltrates were analyzed by flow cytometry in 3 to 5 tissue specimens per patient. Results: The frequency of CD8+ T cells in the total CD45+ infiltrate was highest in normal and CR areas and was significantly reduced in PR vs CR (p<0.01). CXCR3+CD8+ and CD103+CD8+ Tcell frequencies were also reduced in PR vs CR foci (p<0.01, p<0.05, respectively). Meanwhile, the frequency of CXCR3+CD8+ T and CXCR3+++CD8+ T cells was highest and significantly elevated in CR vs normal tissue suggesting enrichment of activated, homing, Tc1 CD8T cells. An increase in total CD8+ and CD103+CD8+ T cells was associated with longer progression-free survival. DESeq2 analysis of bulk mRNA sequencing showed enrichment of CD8a and ITGAE (CD103) gene expression differential in CR vs PR lesions (p=0.028, p=0.00029, respectively). CD8a expression was reduced in panCK- AOI of resistant (PR) foci by GeoMx WTA spatial transcriptomic analysis in two model patients with multi-focal tumors. Flow analysis of EpCAM+ cells had a significant increase in B7H3 expression in PR vs CR lesions (p<0.05). We are currently integrating analysis of myeloid cells and expand spatial transcriptomic analysis of matched multi-focal tumors to further dissect patterns of therapeutic response in our study cohort. Conclusions: In conclusion, PSMA /PET and mpMRI based precision sampling of tumor tissue associated with differential therapeutic response patterns captured differences in the TIME infiltrates and these observations may provide hypothesis to test biological mechanisms to expedite discovery of targetable mechanisms to improve tumor stratification and targeting in high-risk prostate cancer. Citation Format: Erika Heninger, Jamie M. Sperger, Kristin Weinstein, Brian P. Johnson, Peter G. Geiger, Shane A. Wells, Steve Y. Cho, Wei Huang, Philippos Tsourkas, Sean McIlwain, Irene M. Ong, David Quigley, David F. Jarrard, Sheena C. Kerr, David J. Beebe, Joshua M. Lang. Differential Patterns of Immune Infiltration in the Tumor Immune Microenvironment Associate with Therapeutic Response in Primary Prostate Cancer Following Chemohormonal Therapy [abstract]. In: Proceedings of the AACR Special Conference in Cancer Research: Innovations in Prostate Cancer Research and Treatment; 2026 Jan 20-22; Philadelphia PA. Philadelphia (PA): AACR; Cancer Res 2026;86(2_Suppl):Abstract nr A023.

  PublisherDOI

• Lymphatic Endothelial Cells Regulate Neutrophil Phenotypes and Function in a Microphysiological Model of Infection

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-03-27

  articleOpen accessSenior authorCorresponding

  ABSTRACT Early skin inflammation requires coordinated immune regulation, with neutrophils acting as first-line responders. While the blood vasculature and its role in neutrophil recruitment during infection has been extensively studied, the lymphatic system remains comparatively understudied despite its known role in immune cell trafficking. Growing evidence suggests lymphatic vessels actively participate in regulating inflammatory responses, yet whether they coordinate neutrophil behavior during skin infection remains unclear. Staphylococcus aureus is particularly problematic in this context, employing multiple immune evasion strategies and representing a major driver of antibiotic-resistant skin and soft tissue infections worldwide. To address this gap, we developed a human-based 3D microphysiological system incorporating luminal lymphatic endothelial vessels, a collagen matrix and bacteria to model an infected microenvironment. We evaluated neutrophil migration, phagocytosis and NETosis in response to Escherichia coli and S. aureus . Lymphatic endothelium amplified neutrophil migration in a bacterial-dependent manner, with E. coli promoting directional migration toward the vessel while S. aureus suppressed migration and directionality despite increased phagocytic uptake. S. aureus also induced myeloperoxidase-positive NETs with nuclear morphology consistent with vital NETosis, rescued by DNase treatment. To our knowledge, this is the first demonstration that lymphatic endothelium directly drives neutrophil behavior during skin infection.

  PublisherOA PDFDOI

• Prostate Cancer-Associated Fibroblasts: A Review on CAF Functions, Heterogeneity, Resistance Mechanisms, and Future in a Chip

  International Journal of Molecular Sciences · 2026-02-05 · 1 citations

  articleOpen access

  Cancer-associated fibroblasts (CAFs) are key regulators of the prostate tumor microenvironment (TME) with influence on disease progression and therapeutic response. CAFs originate from multiple precursors and retain remarkable plasticity while tumors evolve. Therefore, the CAF pool displays considerable functional heterogeneity, which is well-reflected in complex molecular signatures. However, overlapping biomarker patterns with other stromal subsets make it challenging to identify and assess the role of specific CAF subpopulations. Through reciprocal tumor-stroma interactions, CAFs promote extracellular matrix (ECM) remodeling, angiogenesis, metabolic reprogramming, and immune evasion, collectively fostering an adaptive niche that supports tumor survival, though some CAF subsets have been shown to support anti-tumor response. In prostate cancer (PCa), CAFs promote resistance to androgen receptor pathway inhibitor therapy, chemotherapy, and radiotherapy, emphasizing their potential value as therapeutic targets. However, CAF targeting has shown limited clinical benefit in PCa, due to complex, context-dependent CAF functions that make it challenging to exploit this unique stromal population for therapeutic gain. Recent advances in organ-on-a-chip (OOC) models offer new opportunities to investigate the mechanisms behind TME interactions and evaluate CAF-targeted strategies in physiologically relevant fully humanized environments. This review provides current insights into CAF heterogeneity and therapy resistance in PCa and highlights emerging translational OOC models to guide the development of more effective therapies to disrupt the TME.

  PublisherOA PDFDOI

• Abstract A031: Targeting prostate cancer bone metastasis with iNKT immunotherapy

  Cancer Research · 2026-01-20

  article

  Abstract Introduction: For men with metastatic castration resistant prostate cancer (mCRPC), there is an urgent need for improved therapeutics as the disease is highly lethal. Approximately 90% of mCRPC patients develop bone metastases. The bone tumor microenvironment (TME) is highly complex, involving dynamic interactions between tumor cells and bone-resident stromal populations that drive pathological remodeling, therapy resistance and create immunosuppression. Invariant natural killer T cells (iNKT cells) are a subset of “donor unrestricted” T cells that do not mediate alloreactivity and have strong potential as off-the-shelf immunotherapy agents. iNKT cells home to bone marrow and have been shown to modulate the bone TME in addition to directly killing tumor cells. To further investigate the mechanisms of iNKT modulation of the prostate cancer (PCa) bone TME, we used a microphysiological system (MPS), an advanced fully human 3D in vitro culture model that recreates the PCa bone microenvironment. Methods: The bone MPS includes 9 different primary cell types cultured in an optimized media formulation. The MPS comprises a main chamber filled with a collagen matrix containing osteoblasts, osteoclasts, adipocytes, mesenchymal stem cells, macrophages, fibroblasts, and PCa organoids, surrounding an engineered blood vessel mimic. iNKT cells were embedded within the bone stroma or added through the endothelial microvessel for trafficking readouts. MPS were analyzed using fluorescence microscopy to evaluate tumor cell viability (calcein-AM/ethidium homodimer), and trafficking of iNKT cells into the TME from the vasculature. Media was removed from the MPS for cytokine secretion analysis using multiplex bead-based ELISA and RNA was isolated from cells for gene expression analysis using qPCR. Results: We demonstrated that iNKT cells migrated into the bone TME from the vasculature, with migration increased in the presence of PCa tumor organoids. iNKT cells invaded into the tumor organoids and induced tumor cell death. Co-culture experiments demonstrated that this iNKT cell mediated tumor cell death was dependent on the presence of osteoclasts. qPCR revealed upregulation of FasL and chemokines CCL2, CCL4, CXCL9, and CXCL11 in the iNKT condition compared to control, suggesting activation of M1-type macrophages and induction of FasL-mediated cytotoxicity. Multiplex bead-based ELISA analysis showed upregulation of M-CSF, GM-CSF, G-CSF, IL-1α, TNFα, MIP-1α, IL-2, IL-9, MCP-3, and RANTES, consistent with enhanced pro-inflammatory reprogramming, and recruitment of effector immune cells. Conclusions: These findings suggest that iNKT cells are a promising immunotherapy for treatment of PCa bone metastases. In addition to killing tumor cells, iNKT cells can modulate the PCa bone metastatic niche which could contribute towards overcoming tumor-induced immunosuppression and promoting anti-tumor immunity. Citation Format: Cristina Sánchez-de-Diego, Nikhila S. Bharadwaj, Marcos Lares, Nikolett Lupsa, Erika Heninger, Joshua M. Lang, David J. Beebe, Jenny E. Gumperz, Sheena C. Kerr. Targeting prostate cancer bone metastasis with iNKT immunotherapy [abstract]. In: Proceedings of the AACR Special Conference in Cancer Research: Innovations in Prostate Cancer Research and Treatment; 2026 Jan 20-22; Philadelphia PA. Philadelphia (PA): AACR; Cancer Res 2026;86(2_Suppl):Abstract nr A031.

  PublisherDOI

• Confinement by Liquid‐Liquid Interface Replicates In Vivo Neutrophil Deformations and Elicits Bleb‐Based Migration

  Advanced Science · 2025-03-28 · 4 citations

  articleOpen accessSenior authorCorresponding

  Leukocytes forge paths through interstitial spaces by exerting forces to overcome confining mechanical pressures provided by surrounding cells. While such mechanical cues regulate leukocyte motility, engineering an in vitro system that models the deformable cellular environment encountered in vivo has been challenging. Here, microchannels are constructed with a liquid-liquid interface that exerts confining pressures similar to cells in tissues, and thus, is deformable by cell-generated forces. Consequently, the balance between migratory cell-generated and interfacial pressures determines the degree of confinement. Pioneer cells that first contact the interfacial barrier require greater deformation forces to forge a path for migration, and as a result migrate slower than trailing cells. Critically, resistive pressures are tunable by controlling the curvature of the liquid interface, which regulates motility. By granting cells autonomy in determining their confinement, and tuning environmental resistance, interfacial deformations match those of surrounding cells in vivo during interstitial neutrophil migration in a larval zebrafish model. It is discovered that neutrophils employ a bleb-based mechanism of force generation to deform a soft barrier exerting cell-scale confining pressures. In all, this work introduces a tunable in vitro material interface that replicates confining pressures applied by soft tissue environments.

  PublisherOA PDFDOI

• Modeling Toxoplasma gondii-gut early interactions using a human microphysiological system

  PLoS neglected tropical diseases · 2025-02-04 · 3 citations

  articleOpen accessCorresponding

  Oral transmission of parasites via environmentally resistant cyst stages in contaminated food or water is a common route of human infection, but there are no effective vaccines available for any enteric parasitic infection. Our knowledge of parasite cyst stage conversion and interaction with the intestinal tract is limited. Here, we investigate infection dynamics of Toxoplasma gondii cyst-stage in murine jejunum and human intestinal microphysiological systems. We focus on parasite ingress, replication, and conversion of the cyst stage to the rapidly replicating dissemination stage. In vivo bioluminescent imaging of mice fed cysts revealed spots of infection throughout the jejunum and ileum, which were selected for further analyses. Immunostaining showed parasite migration and replication predominantly in the stroma, with minimal replication in enterocytes. We recapitulated bradyzoite infection in human intestinal microphysiological systems and showed stage conversation and migration through collagen. This integrated approach elucidates complex host-parasite interactions, highlighting the value of microphysiological systems in advancing understanding and identifying potential therapeutics.

  PublisherDOI

Recent grants

• NIH Grant R21CA122672

  NIH · $344k · 2010

• Cancer Center Administration

  NIH · $99.8M · 1997–2028

• NIH Grant R01CA185251

  NIH · $2.9M · 2019

• An automated high-throughput tissue model for screening metastatic effectors

  NIH · $3.1M · 2015–2019

• Mechanisms of microenvironment mediated resistance to cancer cell surface targeted therapeutics

  NIH · $1.6M · 2020–2022

Frequent coauthors

• Joshua M. Lang

  146 shared

• Melissa C. Skala

  Morgridge Institute for Research

  137 shared

• José M. Ayuso

  University of Wisconsin–Madison

  133 shared

• Erwin Berthier

  University of Washington

  108 shared

• Marı́a Virumbrales-Muñoz

  University of Wisconsin Carbone Cancer Center

  99 shared

• Scott M. Berry

  University of Kentucky

  90 shared

• Kyung E. Sung

  United States Food and Drug Administration

  79 shared

• David J. Guckenberger

  70 shared

Education

• Ph.D., Pathology

  University of Wisconsin-Madison

  1990

• M.D., Medicine

  University of Wisconsin-Madison

  1985

• B.S., Biology

  University of Wisconsin-Madison

  1981