About

Tao Liu is a Professor of Biostatistics and the Director of the Online Master’s Program in Biostatistics at Brown University. He obtained his PhD in Biostatistics from the University of Pennsylvania. His research interests are in health data science, including clinical decision-making, incomplete data problems, causal inference, diagnostic testing, and the design of clinical trials. Dr. Liu is also a faculty member at the biostatistics core of the Lifespan/Boston/Brown Center for AIDS Research (CFAR), the Brown Data Science Institute (DSI), and the Advance-Clinical Translational Research (Advance-CTR). Additionally, he is an affiliated faculty member for the AMPATH Biostatistics and Data Program. His work focuses on applying biostatistical methods to improve health outcomes and understanding complex health data.

Research topics

• Computer Science
• Artificial Intelligence
• Medicine
• Chemistry
• Biology
• Internal medicine
• Pediatrics
• Nuclear medicine
• Chromatography
• Computational biology
• Bioinformatics
• Genetics
• Radiology
• Applied psychology
• Virology
• Psychology
• Pathology

Selected publications

• Performance analysis of a cogeneration system coupled with molten salt heat storage

  Applied Thermal Engineering · 2025-10-18 · 2 citations

  article1st author
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• Gut microbial-derived phenylacetylglutamine accelerates host cellular senescence

  Nature Aging · 2025-01-10 · 55 citations

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• A0767 – Senescence-associated miRNA in clear cell renal cell carcinoma: Exploring the role of the tumor immune microenvironment and predicting survival through senescence-associated factors

  European Urology · 2025-03-01

  articleOpen access
  PublisherDOI

• Understanding Oral Prep Interest Among South African Adolescents: The Role of Perceived Parental Support and PrEP Stigma

  UNC Libraries · 2025-04-18

  articleOpen access
  PublisherDOI

• Enhancing chemosensitivity in pancreatic cancer: Novel strategies to overcome therapeutic resistance

  Oncology and Translational Medicine · 2025-09-01 · 3 citations

  articleOpen access

  Abstract Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive and fatal malignancies, with a 5-year survival rate of <15%. Despite significant advancements in targeted therapies and immunotherapy, these approaches benefit only a limited subset of patients, leaving chemotherapy as the primary treatment modality for most patients. Chemotherapy is an essential adjunct to surgical resection, the only potentially curative option, playing a crucial role in reducing the tumor burden, delaying disease progression, and alleviating symptoms. However, its long-term efficacy is frequently undermined by the development of chemoresistance, wherein tumor cells adopt diverse strategies to evade or repair chemotherapy-induced damage. Addressing this critical barrier is imperative for improving the clinical outcomes of PDAC. This review comprehensively examines the multifaceted mechanisms of chemoresistance in PDAC and highlights innovative strategies designed to enhance chemosensitivity, thereby offering new hope for overcoming these challenges and improving patient survival.

  PublisherDOI

• 816 | FIRST DATA DISCLOSURE FROM PHASE 1B/2 EPCORE NHL‐4: EPCORITAMAB IN CHINESE PATIENTS WITH RELAPSED OR REFRACTORY DIFFUSE LARGE B‐CELL LYMPHOMA

  Hematological Oncology · 2025-06-01

  articleOpen access

  Introduction: DLBCL comprises 38% of all non-Hodgkin lymphoma (NHL) in China, and outcomes for R/R DLBCL are generally poor. Chemoimmunotherapy remains the predominant third-line (3L) treatment (tx), with limited efficacy and suboptimal safety. In China, CAR T tx is approved in 3L but access can be limited, highlighting the need for convenient, tolerable, and efficacious tx options for R/R DLBCL. Subcutaneous (SC) epcor is a CD3xCD20 bispecific antibody approved globally, including the EU, for R/R DLBCL and follicular lymphoma (FL). Here we present the first efficacy and safety data from R/R DLBCL Chinese pts treated with epcor monotherapy in the pivotal EPCORE NHL-4 (NCT05201248) trial. Methods: Pts had R/R NHL with ≥ 2 lines of prior systemic tx and were administered 48 mg epcor SC in 28-day cycles (C): QW, C1–3; Q2W, C4–9; Q4W, C10+ until disease progression or unacceptable toxicity. In C1, step-up dosing (day [D] 1, 0.16 mg; D8, 0.8 mg; D15, D22, 48 mg) and prophylactic corticosteroids were used to prevent cytokine release syndrome (CRS). Key endpoints included tx-emergent adverse events (TEAEs), response rates (overall response rate [ORR]/complete response rate [CRR]) and progression-free survival (PFS) by independent review committee (IRC), and duration of response (DoR/DoCR) by IRC. Results: As of June 19, 2024, 42 pts were enrolled (3 DLBCL, 2 FL in safety run-in; 37 DLBCL in dose expansion). In dose expansion, median age was 57.0 y and pts received ≥ 1 epcor dose; median follow-up was 18.5 mo. In dose expansion, 73% of pts had advanced disease (Ann Arbor Stage III–IV), 89% had primary refractory disease, and 65% were refractory to the last line of anti-CD20 tx. Median prior lines of tx was 3 (range, 2–7). Most pts (97%) had ≥ 1 Grade (G) 3/4 TEAE, most commonly lymphopenia (89%), neutropenia (57%), leukopenia (35%), and thrombocytopenia (22%). CRS was reported in 84% of pts: G1 51%, G2 32%, and no G ≥ 3. Most CRS events occurred after the first full dose (C1D15), with median time to onset of 16 D (range, 2–29). All CRS events resolved and no pts discontinued epcor due to CRS. No pts had immune effector cell-associated neurotoxicity syndrome, and 1 pt (3%) had G3 clinical tumor lysis syndrome that resolved without dose interruption. Three fatal TEAEs were all due to progressive disease and unrelated to epcor. A correlation between depth of response and long-term outcomes was observed. ORR was 65% and CRR was 38%; median DoR, DoCR, and OS were not reached (NR; Table). Conclusions: Epcor, a T cell-engaging bispecific antibody, showed favorable outcomes as monotherapy in Chinese pts with refractory and heavily pretreated R/R DLBCL. High ORR and CRR were achieved early and responses were deep and durable. Safety was manageable and CRS was low grade with predictable timing. Our results are consistent with the pivotal EPCORE NHL-1 and NHL-3 trials and support further development of epcor in China. Research funding declaration: Epcoritamab is being developed in collaboration between AbbVie and Genmab who funded this study and participated in the design of the study, research, analysis, data collection, interpretation of data, reviewing, and approval of the publication. Encore Abstract: ASCO 2025 Keywords: aggressive B-cell non-Hodgkin lymphoma; molecular targeted therapies; indolent non-Hodgkin lymphoma Potential sources of conflict of interest: S. Diness Vindelov Employment or leadership position: Employee and stock shareholder of Genmab T. Yin Employment or leadership position: Employee and stock shareholder of AbbVie X. Chen Employment or leadership position: Employee and stock shareholder of AbbVie C. Moureaud Employment or leadership position: Employee and stock shareholder of AbbVie T. Jiang Employment or leadership position: Employee and stock shareholder of AbbVie

  PublisherOA PDFDOI

• Somatic <i>TYK2</i> activating mutations in tumor-infiltrating T cells promote anti-cancer immunity

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-10-15 · 1 citations

  preprintOpen access

  Abstract Cancer cells evolve to increase fitness and evade the immune system, but it is not clear if tumor infiltrating lymphocytes (TILs) undergo selection for somatic mutations that augment anti-cancer immunity. Using single molecule whole exome sequencing in TILs, we identified somatic mutations in Tyrosine-protein kinase 2 ( TYK2 ), several of which increased TYK2 phosphorylation, JAK-STAT signaling, and interferon gamma signaling. Among these mutations, TYK2 D810V was recurrently observed in patients with diverse cancer types. In vitro, TYK2 D810V enhanced T cells effector functions and cytokine production. We generated mice with a germline Tyk2 D807V mutation that recapitulated the human TYK2 D810V mutation. These mice were healthy and did not develop autoimmune disorders. However, they possessed enhanced anti-tumor effects in the context of syngeneic and autochthonous cancer models. Adoptive therapy with Tyk2 D807V CD8⁺ T cells also decreased cancer growth. Thus, naturally occurring mutations in non-malignant lymphocytes can antagonize cancer and inspire new immunotherapies strategies.

  PublisherOA PDFDOI

• The Prevalence and Associated Factors of HIV Self-Testing Among High-Risk Men Who Have Sex with Men in China: A Study Based on Bayesian Network Model

  Archives of Sexual Behavior · 2025-07-01

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• SpyTag-PEGylated probiotics delivering IL-1Ra modulate gut-lung crosstalk to mitigate septic lung injury

  Journal of Controlled Release · 2025-08-23 · 4 citations

  articleCorresponding
  PublisherDOI

• Exosomes in inflammation and cancer: from bench to bedside applications

  Molecular Biomedicine · 2025-06-09 · 20 citations

  reviewOpen access

  Exosomes, lipid bilayer nanovesicles secreted by nearly all cell types, play pivotal roles in intercellular communication by transferring proteins, nucleic acids, and lipids. This review comprehensively summarizes their multiple functions in inflammation and cancer. In inflammation, exosomes exhibit context-dependent pro- or anti-inflammatory effects: they promote acute responses by delivering cytokines and miRNAs to activate immune cells, yet suppress chronic inflammation via immunoregulatory molecules. Two representative inflammatory diseases, namely sepsis and inflammatory bowel disease, were highlighted to elucidate their roles in the acute and chronic inflammatory diseases. In cancer, exosomes orchestrate tumor microenvironment (TME) remodeling by facilitating angiogenesis, metastasis, and immune evasion through interactions with cancer-associated fibroblasts, tumor-associated macrophages, and extracellular matrix components. Furthermore, exosomes can facilitate the transition from inflammation to cancer by impacting pertinent signaling pathways via their transported oncogenic and inflammatory molecules. Tumor-derived exosomes also serve as non-invasive biomarkers correlating with disease progression. Clinically, exosomes demonstrate promise as therapeutic agents and drug carriers, evidenced by ongoing trials targeting inflammatory diseases and cancers. However, challenges in isolation standardization, scalable production, and understanding functional heterogeneity hinder clinical translation. Future research should prioritize elucidating cargo-specific mechanisms, optimizing engineering strategies, and advancing personalized exosome-based therapies. By bridging molecular insights with clinical applications, exosomes hold great potential in precision medicine for inflammation and oncology.

  PublisherOA PDFDOI

Recent grants

• Addressing alcohol misuse in HIV prevention and care: The Brown University Alcohol Research Center on HIV (ARCH)

  NIH · $39.3M · 2010–2026

Frequent coauthors

• Roland C. Merchant

  115 shared

• Brandon D. L. Marshall

  Brown University

  42 shared

• Theresa I. Shireman

  Providence College

  42 shared

• Anna E. Wentz

  VA New Jersey Health Care System

  42 shared

• Curt G. Beckwith

  Brown University

  39 shared

• Ralph C. Wang

  University of California, San Francisco

  39 shared

• Kenneth H. Mayer

  Fenway Health

  35 shared

• Susan Cu‐Uvin

  Brown University

  28 shared

Education

• Ph.D., Biostatistics

  University of Pennsylvania