About

Eugene Yuejin Wang is the Abby Aldrich Rockefeller Professor of Asian Art at Harvard University and the founder and director of Harvard FAS CAMLab. His extensive publications range from early Chinese art and archaeology to modern and contemporary Chinese art and cinema. His book, Shaping the Lotus Sutra: Buddhist Visual Culture in Medieval China (2005), explores Buddhist worldmaking and received the Sakamoto Nichijin Academic Award from Japan. His current research focuses on the cognitive study of art and consciousness as well as biocentric art that integrates visual, biological, and ecological systems. As the founding director of Harvard FAS CAMLab, he explores the nexus of cognition, aesthetics, and mindscape, leading projects that investigate multimedia storyliving and immersive artistic and spiritual experiences, integrating humanistic research with sensorial media practice.

Research topics

• Biology
• Machine Learning
• Computer Science
• Mathematics
• Food science
• Chemistry
• Medicine
• Horticulture
• Statistics
• Internal medicine
• Cancer research

Selected publications

• Tumor-targeted Butein-loaded PLGA nanoparticles improve gemcitabine sensitivity and prolong survival in pancreatic ductal adenocarcinoma

  Genes & Diseases · 2026-04-01

  articleOpen access

  Pancreatic ductal adenocarcinoma (PDAC) remains one of the most lethal cancers, marked by late-stage diagnosis, a dense stromal microenvironment, and the rapid emergence of chemoresistance. Gemcitabine (Gem) monotherapy offers limited survival benefits, highlighting the urgent need for novel therapeutic approaches. We developed tumor-targeted Butein-loaded PLGA nanoparticles (TP-PLGA-B) to enhance drug delivery and evaluate their synergistic effects with Gem in PDAC models. Nanoparticles were characterized by size, stability, and drug release profiles. Biological efficacy was assessed through in vitro cytotoxicity, migration, colony formation assays, and in vivo therapeutic studies in a syngeneic orthotopic PDAC mouse model. TP-PLGA-B nanoparticles (∼170 nm) demonstrated pH-sensitive drug release and selective tumor targeting. Combination therapy with TP-PLGA-B and low-dose Gem significantly reduced the IC 50 by 2.5–6.2-fold compared with controls and was more synergistic than free drug combinations, inhibited EGFR, cMET, and p-STAT3 pathways, and suppressed pro-inflammatory cytokine expression. In vivo , this combination markedly decreased tumor volume, enhanced apoptosis, and extended median survival from 24 to 56 days without noticeable toxicity. Our findings support TP-PLGA-B nanoparticles as a promising strategy to enhance Gem sensitivity, reduce chemoresistance, and improve therapeutic outcomes in PDAC.

  PublisherDOI

• Amphiphilic Glycopolymer Nanoparticles for pH-Responsive Paclitaxel Delivery and Enhanced Efficacy in Pancreatic Ductal Adenocarcinoma Therapy

  ACS Applied Bio Materials · 2026-05-15

  article

  , PCG(PTX) demonstrated selective uptake by PDAC cells and enhanced cytotoxicity. Combination with gemcitabine (Gem) further reduced viability and migration while promoting apoptosis. In orthotopic PDAC mouse models, PCG(PTX) + Gem significantly suppressed tumor growth, prolonged survival, and tolerability compared with free PTX. These results demonstrate the promise of PCG glycopolymer nanoparticles as an effective platform for targeted, combination chemotherapy in PDAC.

  PublisherDOI

• Tumor Treating Fields (TTFields) Potentiate Cisplatin Efficacy and Remodel the Transcriptional Landscape in Preclinical Models of Pancreatic Ductal Adenocarcinoma

  SSRN Electronic Journal · 2026-01-01

  preprintOpen access
  PublisherDOI

• A method for evaluating the hovering accuracy of drone based on visual guidance total station

  2026-01-09

  article1st authorCorresponding

  This study evaluates the positioning accuracy of Unmanned Aerial Vehicles (UAVs) using a visual guidance system integrated with a total station. Traditional total station measurements face challenges in image readability and limited zoom range, prompting the adoption of visual target detection and automated search techniques. The proposed method employs a two-axis turntable-mounted zoom camera to capture initial angular and vertical adjustments, enabling approximate coordinate calculation of a reflector plate on the UAV. Through coordinate transformation using extrinsic parameters, these values are converted into the total station’s framework, where precise distance measurements (via Distance Measurement Engine) and angle decomposition refine spatial positioning. Experimental results demonstrate a hovering accuracy of approximately 35.2 mm (1σ) at 30 m altitude, with 3D coordinate data showing standard deviations of 28.2 mm (X), 33.4 mm (Y), and 35.1 mm (Z). These findings validate the system’s capability to achieve reliable, high-precision UAV localization under visual guidance, supporting applications in surveying, construction, and automated machinery alignment.

  PublisherDOI

• Surface-engineered dual drug-loaded tumor-targeted liposomal nanoparticles to overcome the therapeutic resistance in glioblastoma multiforme

  Communications Medicine · 2026-03-18 · 1 citations

  articleOpen access

  Glioblastoma (GBM) is the most common high-grade primary malignant brain tumor, characterized by a notably poor prognosis. Current treatments for GBM have shown limited effectiveness in improving patient survival, highlighting the urgent need for effective therapeutic strategies. Combination therapy offers significant potential in overcoming resistance by targeting multiple signaling pathways; however, it often comes with increased toxicity compared to monotherapy. Co-encapsulating multiple therapeutic agents into a tumor-targeted drug delivery platform holds promise for overcoming these limitations and improving treatment outcomes. We developed a tumor-targeted liposomal nanoformulation (TTL) using phospholipids, cholesterol, DSPE-(PEG)2000-OMe, and a proprietary tumor-targeting peptide (TTP). The TTL was loaded with everolimus (TTL-E), vinorelbine (TTL-V), rapamycin (TTL-R), a combination (TTL-EV), or (TTL-RV). These formulations were tested in vivo on orthotopic GBM mice, combined with temozolomide and radiation. RNA sequencing was performed to identify molecular and transcriptome changes post-treatment. TTL demonstrated tumor-specific uptake, effectively delivering drugs to GBM tumors. TTL-EV and TTL-RV outperformed single-drug formulations. Radiation combined with TTL-EV/RV improved tumor growth inhibition and survival, while temozolomide provided minimal benefit. Transcriptome analysis revealed differentially expressed genes (DEGs) linked to DNA damage repair, cell cycle, metabolism, and extracellular matrix pathways. TTL crossed the blood-brain barrier, targeting tumors effectively. Radiation plus TTL-EV/RV enhanced tumor suppression and survival in GBM models. Gene expression analysis identified DEGs related to DNA damage and cell death. Mechanistic studies suggest TTL-EV plus radiation inhibits mTOR/MAPK pathways and sensitizes tumors to radiation. These findings offer a potential approach for improving GBM treatment. Glioblastoma (GBM) is the most aggressive type of brain cancer and is very hard to treat. Current treatments such as surgery, radiation, and chemotherapy often do not work well enough, and patients usually survive for only a short time. One reason is that GBM tumors can resist treatment. Using more than one drug together may help, but it often causes harmful side effects. In this study, we created a new way to deliver drugs directly to brain tumors. We designed very small carriers, called tumor-targeted liposomes (TTL), that can travel into the brain and release drugs inside the tumor. We tested TTL loaded with different combinations of two cancer drugs in mice with GBM, together with radiation therapy. We found that this new treatment reached the brain tumors and worked better than single drugs. The combination slowed tumor growth and helped the mice live longer. Importantly, the new therapy also made tumors more sensitive to radiation. These findings suggest that this drug delivery system could be a promising new approach for treating GBM and may lead to better outcomes for patients in the future. Angom, Rachamala et al. developed a tumor-targeted liposomal nanoformulation using phospholipids, cholesterol, DSPE-(PEG)2000-OMe, and tumor-targeting peptide. The nanoformulation combined with radiation improved survival in mouse models of glioblastoma.

  PublisherOA PDFDOI

• Strategic trimodal therapy enhances radiation-induced abscopal response in renal cancer

  Journal of Translational Medicine · 2025-12-02 · 2 citations

  articleOpen access

  The abscopal effect, tumor regression at distant, non-irradiated sites following localized radiotherapy, is rarely observed, even in immunogenic cancers such as renal cell carcinoma. Current strategies have largely failed to reliably enhance this phenomenon. This study aimed to develop and evaluate a novel therapeutic approach to potentiate the abscopal effect using a combination of tumor-targeted liposomal everolimus and YM155 (EY-L), radiation, and interleukin-2 (IL-2). A trimodal therapy comprising EY-L, localized radiation, and systemic IL-2 was tested in two murine renal cancer models (Renca and LVRCC67) using a bilateral tumor setup to distinguish local and distant tumor responses. The efficacy of the triple therapy was compared to that of single and dual combinations. Downstream analyses including immunohistochemistry, CD8+ T cell depletion, and spatial transcriptomics were performed to investigate potential mechanisms underlying the observed effects. In the Renca model, the EY-L + R + IL-2 triple combination significantly suppressed growth in both irradiated and non-irradiated tumors, demonstrating a robust enhancement of the abscopal effect. Dual combinations failed to elicit similar systemic responses, underscoring the necessity of the full triple regimen. Mechanistic analyses revealed increased infiltration of CD8⁺ T cells and reduced CD163+ macrophages in non-irradiated tumors, suggesting that enhanced systemic anti-tumor immunity mediates the effect. The LVRCC67 model showed similar trends, however the effects were modest, likely attributable to difference in immune responsiveness. This study presents a novel and effective strategy to induce the abscopal effect through a synergistic combination of targeted drug delivery, radiotherapy, and immunotherapy. The approach offers strong translational potential for improving radioimmunotherapy outcomes in renal and potentially other immunogenic cancers.

  PublisherDOI

• Surface-engineered dual drug-loaded tumor-targeted liposomal nanoparticles to overcome the therapeutic resistance in glioblastoma multiforme

  Research Square · 2025-10-31

  preprintOpen access
  PublisherOA PDFDOI

• VEGF-B/NRP1 Signaling Modulates Mitochondrial Homeostasis and Cardiac Function After Myocardial Infarction

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-04-20

  preprintOpen access

  Abstract Background Myocardial infarction (MI) remains a leading cause of mortality worldwide. Recent studies suggest a cardioprotective role for vascular endothelial growth factor-B (VEGF-B) in MI. However, the molecular mechanisms of VEGF-B-mediated signaling via its co-receptor Neuropilin-1 (NRP1) in MI are poorly understood. In this study, we investigated the intricate signaling mechanisms involving VEGF-B and NRP1 in cardiomyocytes (CMs) using ischemic injury as a model of MI. And secondly, we further validated the protective role of VEFG-B in ischemic heart disease, shedding light on their roles not only in cardiac function but also in its therapeutic potential. Methods In this study, we utilized both in vitro and in vivo approaches to elucidate the role of VEGF-B and NRP1 signaling in MI and how it manifests a protective role in mitochondrial functions and cardiac regeneration following ischemic injury. We used two different cardiomyocyte cell lines, H9c2 (rat ventricular cardiomyocytes) and HL-1 (mouse ventricular cardiomyocytes), and induced hypoxia conditions, using either 1% oxygen or 200µM cobalt chloride (CoCl 2 ) to mimic the myocardial infarction-induced ischemic injury in the heart. In addition, we developed a novel heat shock inducible zebrafish model of a cardiomyocyte-specific VEGF-B overexpression system to further examine the protective role of VEGF-B in vivo . Results Our findings indicate that both VEGF-B and NRP1 are predominantly expressed in heart tissue compared to other tissues, and their expression is altered in response to hypoxia/ischemic injury. Our results demonstrate that VEGF-B treatment prior to hypoxia enhances cardiomyocyte survival, while NRP1 knockdown abolishes this protective effect, highlighting a prominent role of NRP1 signaling in VEGF-B-mediated cardio protection. Furthermore, we found that VEGF-B promotes cardiomyocyte survival by improving mitochondrial function, as evidenced by reduced oxidative stress and ROS accumulation, decreased oxidative stress, preserved mitochondrial membrane potential, and increased ATP levels. Lastly, using our VEGF-B transgenic zebrafish model, we demonstrated that VEGF-B overexpression in zebrafish cardiomyocytes protects the heart from ischemic injury and enhances cardiac regeneration in an NRP1-dependent manner. Conclusion Our study has uncovered an important role of VEGF-B-NRP1 signaling axis in VEGF-B mediated cell survival and in beneficial mitochondrial functions in the CMs. Importantly, we also demonstrated that VEGF-B is protective against ischemic injury in vivo using a novel zebrafish model Novelty and Significance What Is Known? Myocardial infarction (MI) results in mitochondrial dysfunction, cardiomyocyte death, and adverse ventricular remodeling. Vascular Endothelial Growth Factor B (VEGF-B) is traditionally associated with cardiac metabolism, survival, vascular biology, particularly in angiogenesis and lipid metabolism. The neurophilin-1 (NRP1) receptor, a co-receptor for VEGF-B, is expressed in cardiomyocytes and implicated in mitochondrial signaling pathways. Emerging evidence suggests that VEGF-B may influence mitochondrial integrity and function under stress conditions. What New Information Does This Article Contribute? VEGF-B exerts a protective effect on cardiomyocyte mitocondria following ischemic injury by preserving mitochondrial function and reducing oxidative stress. NRP1 receptor as a key mediator of VEGF-B modulates mitochondrial homeostasis in cardiomyocytes. VEGF-B signaling can attenuate apoptosis and enhance mitochondrial bioenergetics post-MI, suggesting a novel cardioprotective mechanism. Clinical Implication: These findings suggest that therapeutic strategies aimed at enhancing VEGF-B/NRP1 signaling may improve mitochondrial function and cardiac recovery after MI, offering a novel avenue for limiting heart failure progression in ischemic heart disease.

  PublisherOA PDFDOI

• Abstract 1834: Tumor treating fields (TTFields) plus chemotherapy abrogates pancreatic ductal adenocarcinoma (PDAC) proliferation and alters the tumor microenvironment

  Cancer Research · 2025-04-21

  article

  Abstract Background: TTFields are non-invasive and novel treatment modality that utilizes low intensity, alternating, and intermediate frequency electrical fields to inhibit cancer cell proliferation through a multitude of mechanisms. These include inhibition of mitosis, disruption of cancer cell membranes, metabolomic dysregulation of cancer cells, and immunogenic activation of the tumor microenvironment (TME). TTFields are approved in glioblastoma multiforme, non-small cell lung cancer and malignant mesothelioma. The PANOVA2 trial demonstrated promising efficacy for TTFields when applied together with chemotherapy in patients with PDAC. Mechanisms of TTFields in PDAC need further delineation. We sought to investigate the efficacy of TTFields in vitro and in vivo in PDAC cell lines and mouse models. Preclinical studies were conducted in concert with an going clinical trial (NCT04605913). Experimental Procedures: Utilizing the inovitro apparatus we studied the effect of TTFields (150kHz, intensity 2.9+0.2 V cm RMS, 37ċ, over 72 hrs) in an array of PDAC (Panc1, KPC, Panc2, and AsPC1) and human pancreatic stellate cells (hPSC) cell lines, alone or together with cisplatin (Cis, 0.1μM) or gemcitabine (Gem, 0.01μM), compared to control. Cell viability analysis was conducted in each of the groups. In addition, cell lysates from Panc1 cells from concomitant treatment of TTFields plus Gem were probed for STAT3 and α-SMA to analyze stromal proteins and RAS pathway components (KRAS, P38, P42, and others) were performed via Westen Blot. We also performed RNA sequencing for the different groups to analyze gene expression levels. We further assessed the effect of TTFields (150kHz, intensity 1.8-2 V/cm RMS, over 2 weeks) using the inovivo system with and without chemotherapy (Cis, 0.25 mg/Kg per dose (i.p.) 3 times a week) compared to control in C57BL6 orthotopic murine models (6-7 weeks old C57BL6 mice). Summary of Results: Our analysis revealed statistically significant abrogation of PDAC cancer cell lines for the different groups and hPSC cell viability when compared to control for TTFields monotherapy (p <0.001) and TTFields concomitantly with Gem or Cis (p <0.0001). Western blot analysis demonstrated that TTFields alone and when combined with chemotherapy alters both the stroma and RAS pathways with confirmed downregulation of pSTAT3 and α-SMA and KRAS, P-P38, and P-P42. In vivo analysis revealed significant decrease in tumor volume and weight for the concomitant effect of TTFields + Cis. Conclusion: Our preclinical studies demonstrated the efficacy of TTFields as monotherapy and concomitantly with chemotherapy in PDAC and hPSC cell lines and mouse models. Mechanistic insights from the pre-clinical studies will inform the design of future TTFields studies in PDAC. Citation Format: Hani M. Babiker, Santanu Bhattacharya, Douaa Albelal, Shamit Kumar Dutta, Enfeng wang, Debabrata Mukhopadhyay. umor treating fields (TTFields) plus chemotherapy abrogates pancreatic ductal adenocarcinoma (PDAC) proliferation and alters the tumor microenvironment [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 1834.

  PublisherDOI

• Vascular Endothelial Growth Factor B Modulates Cardiac Functions via Ferroptosis Pathways in Post-Myocardial Infarction

  Cells · 2025-10-21

  articleOpen access

  Myocardial infarction (MI) remains a leading cause of mortality worldwide, yet effective cardioprotective strategies remain limited in clinical settings. Vascular endothelial growth factor B (VEGFB) has emerged as a promising therapeutic candidate in MI, but the role of its co-receptor, Neuropilin-1 (NRP1), in cardiomyocyte (CM) survival under ischemic stress remains poorly understood. Here, we investigated VEGFB-NRP1 signaling using an in vivo zebrafish model of cardiac injury as well as in vitro hypoxia models in CMs. We demonstrated that VEGFB overexpression conferred protection against ischemic injury and enhanced cardiac regeneration in the zebrafish heart. Mechanistically, we showed that VEGFB treatment enhances CM viability through reducing reactive oxygen species (ROS), ferroptosis activation, and preserving mitochondrial integrity. We also demonstrated that NRP1 knockdown in the CMs abolished the VEGFB-mediated protective effects, indicating the significant role of NRP1 signaling in VEGFB-induced cardioprotective effects in MI. Lastly, using transcriptome analysis, we confirmed that VEGFB induces anti-apoptotic and anti-ferroptosis gene programs in CMs in response to hypoxic stress. Collectively, our findings provide mechanistic insight into cell death activation pathways, including ferroptosis, in response to ischemic stress and further validate the therapeutic potential of VEGFB in promoting CM survival in ischemic heart disease.

  PublisherOA PDFDOI

Frequent coauthors

• Debabrata Mukhopadhyay

  Nemours Children's Clinic

  241 shared

• Shamit K. Dutta

  Jacksonville College

  188 shared

• Krishnendu Pal

  Mayo Clinic in Florida

  115 shared

• Phillip Zhe Sun

  107 shared

• Jerry S. Cheung

  Queen Mary Hospital

  105 shared

• Luke H. Hoeppner

  University of Minnesota

  90 shared

• Ying Cao

  Yangzhou University

  73 shared

• Ramcharan Singh Angom

  Jacksonville College

  72 shared

Education

• Ph.D., History of Art and Architecture

  Harvard University

  2007

• M.A., History of Art and Architecture

  Harvard University

  2003

• B.A., History of Art and Architecture

  Harvard University

  2001

Awards & honors

• Guggenheim Fellow (2005)
• Sakamoto Nichijin Academic Award from Japan