
Mark Brown
· Clinical Professor of MarketingVerifiedDuke University · Operations Management
Active 1973–2026
About
Mark T. Brown is the Director of Working Professional Programs at the Management Communication Center at Duke University's Fuqua School of Business. He has been a member of the Fuqua faculty since 1989, teaching Management Communication core courses and advanced electives across various programs including daytime, weekend, and evening MBA programs, as well as full-time MQM and MMS programs, and online MSQM Health Analytics and Business Analytics programs. He has also contributed to the development of effective managers through Fuqua's Executive Education division. In 1992, Mark created the program in Business, Communication, and Culture (BCC), designed to assist international students in their transition to full-time MBA, MQM, and MMS programs in the U.S. Additionally, he works with teams in all of the Executive MBA programs to enhance their effectiveness as dynamic, transformational learning teams. With over thirty years of experience, Mark has served as a consultant to individuals and businesses on communication and strategic leadership topics, including executive leadership styles, crisis communication, cross-cultural communication, effective business presentations, advocacy, team communication, strategic project communication, and situational leadership styles. He has also assisted start-ups in refining business plans and securing funding. Mark completed his undergraduate studies at Georgetown University in international relations and English, earned a master's degree in educational psychology and administration from Bowling Green, and pursued master's and doctoral work at the University of North Carolina at Chapel Hill in communication, rhetoric, and American culture.
Research topics
- Biology
- Cancer research
- Internal medicine
- Immunology
- Computer Science
- Oncology
- Medicine
- World Wide Web
- Cell biology
- Virology
- Genetics
- Bioinformatics
Selected publications
Cancer Research · 2026-04-03
articleAbstract Introduction/Rationale: Glioblastoma (GBM) remains refractory to immunotherapy and exhibits low basal IL-12 and IFN-γ levels relative to other solid tumors, reflecting an immunologically quiescent microenvironment. MVR-C5252 is a replication-competent HSV-1 engineered to deliver IL-12 and an anti-PD-1 antibody fragment, coupling oncolysis with Th1 polarization and localized checkpoint blockade to overcome this resistance. Methods: Stage 1 of PuMP (NCT06126744) assessed safety in six adults with recurrent IDH-wildtype GBM treated with a single convection-enhanced intratumoral infusion (5×106 or 1×108 PFU). An Ommaya reservoir enabled CSF sampling at baseline, 1 hour, and 28 days. Serial CSF single-cell RNA sequencing (scRNA-seq) assessed immune cells, and whole-genome sequencing (WGS) quantified ctDNA and viral kinetics. Liquid chromatography-mass spectrometry (LC-MS)-based metabolomics interrogated IFN-γ-linked tryptophan/kynurenine and arginine/NO pathways. Stage 2 (ongoing) incorporates repeat dosing via an implanted pump, and Stage 3 delivers 12 doses in a Bayesian Optimal Interval (BOIN) dose-escalation design, with the selected dose and schedule planned for expansion in Stage 4. Results: Six patients (3M/3F; 50-59 years; KPS 90 in 5, 80 in 1; MGMT unmethylated in 5) were treated in Stage 1. Median PFS was three months and median OS was 6.1 months, with two patients alive at last follow-up. MVR-C5252 was well tolerated (grade 1-2 only) with no PCR-detectable shedding in urine or saliva. scRNA-seq in four patients with CSF from all three timepoints yielded 14,049 high-quality cells and diverse T-cell and myeloid populations. CD8+ subsets included cytotoxic and exhausted states, while CD4+ subsets spanned naïve, memory, effector, and regulatory states. TAM-like microglia and macrophages were also identified. Rapid early IFN-driven activation and monocyte/dendritic-cell recruitment were observed, followed by sustained cytotoxic and myeloid remodeling at 28 days. CD8+ populations showed increased effector states and fewer exhausted cells, while CD4+ T-cell states spanned naïve and helper lineages. Tumor and viral genome kinetics were characterized by WGS, immune-metabolic pathways were quantified by LC-MS-based metabolomics, and integrated CSF-tumor-blood analyses will be presented. Conclusions: Stage 1 demonstrates safety and immunobiological activity of MVR-C5252, with a single infusion inducing immune remodeling that was not sustained. Meaningful antitumor activity is expected to require repeated intratumoral dosing, as planned in Stages 2-4. These findings establish a mechanistic human model in which localized IL-12/anti-PD-1 virotherapy shifts the tumor microenvironment from a quiescent to a Th1-polarized, cytotoxic state, providing a foundation for next-phase efficacy evaluation. Citation Format: Elizabeth Owens, Kelly Hotchkiss, Stevie Threatt, Justin T. Low, Monika Anand, Julia Louw, Melody Goldston, Margaret O. Johnson, Claire Bradbury, James E. Herndon, Gerry A. Grant, David M. Ashley, Anoop P. Patel, Annik Desjardins, Michael C. Brown, Mustafa Khasraw. IL-12/anti-PD-1 armored oncolytic HSV-1 reprograms CNS immunity: Integrated longitudinal immune, genomic, and metabolic CSF profiling in the MVR-C5252 PuMP Trial [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2026; Part 1 (Regular Abstracts); 2026 Apr 17-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(7 Suppl):Abstract nr 7769.
2026-02-03
articleOpen access<p>Supplementary Figure S6. a-c, Extended data relating to Figure 5. Umap of snRNAseq of combined samples from three intervals (see Figure 5D); individual cell types are labeled (a). Umap of cells identified as T cells in a; individual subsets are labeled (see Supplementary Table S2 for extended data) (b). Proportion of cell types identified in a by time point (c). d, e, Gating strategy used (extended data relating to Figure 5E, F).</p>
Viral Microglia Reprogramming Clears Oligomeric Neurotoxic Debris
bioRxiv (Cold Spring Harbor Laboratory) · 2026-04-08
articleOpen accessOwing to pivotal roles in CNS debris clearance and homeostasis, microglia are central targets for the therapy of neurodegenerative diseases. Intricate proximity to neurons, the inherent danger of neuroimmune toxicity, and intrinsically high plasticity and adaptability, impose high hurdles on microglia modulation. Attenuated viruses are being tested extensively against CNS malignancies (i.e., cancer virotherapy); yet, aside from viral vector-mediated payload delivery, virotherapy for non-neoplastic CNS disease remains unexplored. Here we report disseminated targeting of microglia with the highly attenuated polio:rhinovirus chimera, PVSRIPO, that culminated in profound, durable microglia reprogramming. This phenotype, rooted in extended cytoplasmic viral (v)RNA replication, was non-cytopathogenic and did not yield virus progeny or dissemination. vRNA replication in microglia triggered selective interferon (IFN) regulatory factor (IRF) 3/IRF7 transcriptional programs in the relative absence of NFκB-driven proinflammatory cytokine responses and elicited robust phagocytosis of both tumor cells and amyloid-beta. Targeting of microglia with PVSRIPO mediated immunotherapy in a mouse glioma model and the clearance of oligomeric amyloid-beta deposits in an injectable model of neurotoxic amyloid accumulation. This work identifies attenuated virotherapy as an approach to safely and effectively invigorate microglia function in immune surveillance and neurotoxic debris clearance.
E-Cadherin Is an Accurate Target for Fluorescence-Guided Imaging of Lymph Nodes
Current Issues in Molecular Biology · 2026-03-03
articleOpen accessLymph node (LN) dissection is a necessary part of every oncologic surgery in order to provide important information for staging, predicting prognosis and improving survival. To do this, surgical oncologists strive to localize and dissect every pathologically positive LN while avoiding the increased morbidity of removing true negative LNs. The goal is to develop an imaging method to distinguish positive and negative LNs, but a specific biomarker is missing. Thus, our aim is to identify a reliable imaging marker for identifying LNs with lung cancer cells. After screening many epithelial markers, we identified E-cadherin, a membrane protein normally expressed in epithelial cells, including in the lung. To follow up on our potential target, we performed immunofluorescence staining on 48 human LNs with a conjugated anti-E-cadherin monoclonal antibody. Fluorescence was significantly higher in LNs with metastasis, as shown in 48 positive LNs from patients with resected primary lung cancer. There was high fluorescence in both hilar and mediastinal LNs, and in all primary tumor histologies. E-cadherin may be useful for the surgical oncologist for targeted imaging technologies for selecting positive LNs from lung cancer.
A roadmap to competitive preclinical packages
Nature Medicine · 2026-04-17
articleMolecular Imaging and Biology · 2025-10-14
articleOpen accessPURPOSE: Lymph node (LN) excision is critical in oncologic surgery to provide important therapeutic and diagnostic information. LN evaluation helps in staging cancers, predicting prognosis and improving survival. The ultimate wish of a surgical oncologist would be to localize and dissect all pathologically positive LNs while avoiding the morbidity of removing true negative LNs. The goal of our study was to identify a reliable marker for intraoperative molecular imaging of LNs with cancer cells from non-small cell lung cancer versus a LN without. PROCEDURES: We identified Epithelial Cell Adhesion Molecule (EpCAM), a membrane protein normally expressed in epithelial tissues including lung. We performed immunofluorescence staining on human specimens with a conjugated anti-EpCAM monoclonal antibody. RESULTS: Fluorescence was significantly higher in LNs with metastases as shown in 48 positive LNs from patients with resected primary lung cancer. There was high fluorescence in both hilar and mediastinal LNs, and in all primary tumor histologies. CONCLUSIONS: EpCAM may be useful for the surgical oncologist for intraoperative molecular imaging of positive LNs from lung cancer.
2025-04-03
preprintOpen access1st authorCorresponding<p>Related to Figure 5</p>
2025-04-03
preprintOpen access1st authorCorresponding<p>Related to Figure 4</p>
Molecular Imaging and Biology · 2025-07-14
articleOpen accessPURPOSE: Lung cancer is increasingly diagnosed at early stages, but intraoperative localization of early lesions remains challenging. Intraoperative molecular imaging (IMI) aids in localization of tumors during surgery; however, no optical agents are targeted specifically for early-stage lesions. The sodium-glucose cotransporter 2 (SGLT2) has been implicated in early lung carcinogenesis. This study aimed to describe SGLT2 expression in early-stage lung adenocarcinoma (LUAD) and develop and validate a novel SGLT2-targeted near-infrared (NIR) contrast agent, GlucoGlo, for imaging LUAD. PROCEDURES: SGLT2 expression was confirmed by immunohistochemistry (IHC) in human samples. GlucoGlo optical properties were characterized and compared to common NIR dyes. Sensitivity and specificity for SGLT2 were assessed using preclinical in vitro and in vivo mouse models. RESULTS: On IHC, stage I LUAD displayed higher SGLT2 expression than stage II-III LUAD and normal lung tissue. GlucoGlo exhibited similar depth of penetration and resolution to FDA-approved contrast agents. SGLT2-expressing cell lines treated with GlucoGlo displayed higher fluorescence than the control cell line, confirming SGLT2-dependent uptake. Fluorescence increased with both incubation time and GlucoGlo concentration. Glucose and unconjugated GlucoGlo ligand competitively inhibited GlucoGlo in a dose-dependent manner, indicating high affinity and specificity. GlucoGlo selectively accumulated in SGLT2-expressing flank xenografts, with mean SBR of 2.23 and was inhibited by pretreatment with unconjugated GlucoGlo ligand. CONCLUSIONS: These findings support the potential of GlucoGlo as a targeted IMI contrast agent for early-stage LUAD, and they provide a foundation for future in vivo studies and translational development.
2025-04-03
preprintOpen access1st authorCorresponding<p>Related to Figure 2</p>
Recent grants
Cancer Immunotherapy Through Intratumoral Activation of Recall Responses
NIH · $187k · 2018–2021
Reviving cancer immune surveillance with CD4 T cell help
NIH · $105k · 2021–2022
Frequent coauthors
- 720 shared
S Williams
- 720 shared
Lachlan MacGregor
Roche (Switzerland)
- 720 shared
William M. O’Brien
- 720 shared
Amelia J. Tomkins
The Heart Research Institute
- 720 shared
Søren Christensen
Institut de Psychiatrie et Neurosciences de Paris
- 720 shared
Cdj Barras
Gosford Hospital
- 720 shared
Dominic Thyagarajan
Alfred Health
- 720 shared
Brian Tress
Education
- 2016
Ph.D., Molecular Genetics and Microbiology
Duke University
- 2009
B.S., A.B., Biology, Chemistry
University of North Carolina at Chapel Hill
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