Bio


Driven by the enthusiasm and curiosity about life science and human disease, I have been working on cancer research for more than 5 years. I focus on developing novel therapeutic targets from tumor microenvironment and uncovering mechanisms of tumor progression, especially with expertise in gastrointestinal tumor biology and tumor microenvironment analysis. Now I'm digging into a field about finding a way to empower immunotherapy by appropriately utilizing radiation therapy.

Professional Education


  • B.S., East China University of Science and Technology, Biology engineering (2016)
  • Ph.D., Shanghai Jiao Tong University, Biology (2021)

Stanford Advisors


Patents


  • Wei-Qiang Gao, Bin Ma, Lu Ji. "China P.Rep. Patent ZL 2019 1 1408316.3 The immunotherapy method for gastric cancer via blocking chemokine CCL28", Shanghai Jiao Tong University, Aug 17, 2021

All Publications


  • CD24 is a Superior Immunotherapeutic Target to PD-1 in a Mouse Model of Helicobacter-Induced Gastric Cancer Gastro Hep Advances Ji, L., Peng, P., Gui, L., Yuan, P., Qian, W., Wang, Y., Gao, W., Ma, B. 2021
  • Blockade of beta-Catenin-Induced CCL28 Suppresses Gastric Cancer Progression via Inhibition of Treg Cell Infiltration CANCER RESEARCH Ji, L., Qian, W., Gui, L., Ji, Z., Yin, P., Lin, G., Wang, Y., Ma, B., Gao, W. 2020; 80 (10): 2004-2016

    Abstract

    Dysregulation of Wnt/β-catenin signaling is frequently observed in human gastric cancer. Elucidation of the tumor immune microenvironment is essential for understanding tumorigenesis and for the development of immunotherapeutic strategies. However, it remains unclear how β-catenin signaling regulates the tumor immune microenvironment in the stomach. Here, we identify CCL28 as a direct transcriptional target gene of β-catenin/T-cell factor (TCF). Protein levels of β-catenin and CCL28 positively correlated in human gastric adenocarcinoma. β-Catenin-activated CCL28 recruited regulatory T (Treg) cells in a transwell migration assay. In a clinically relevant mouse gastric cancer model established by Helicobacter (H.) felis infection and N-methyl-N-nitrosourea (MNU) treatment, inhibition of β-catenin/TCF activity by a pharmacologic inhibitor iCRT14 suppressed CCL28 expression and Treg cell infiltration in the stomach. Moreover, an anti-CCL28 antibody attenuated Treg cell infiltration and tumor progression in H. felis/MNU mouse models. Diphtheria toxin-induced Treg cell ablation restrained gastric cancer progression in H. felis/MNU-treated DEREG (Foxp3-DTR) mice, clarifying the tumor-promoting role of Treg cells. Thus, the β-catenin-CCL28-Treg cell axis may serve as an important mechanism for immunosuppression of the stomach tumor microenvironment. Our findings reveal an immunoregulatory role of β-catenin signaling in stomach tumors and highlight the therapeutic potential of CCL28 blockade for the treatment of gastric cancer. SIGNIFICANCE: These findings demonstrate an immunosuppressive role of tumor-intrinsic β-catenin signaling and the therapeutic potential of CCL28 blockade in gastric cancer.

    View details for DOI 10.1158/0008-5472.CAN-19-3074

    View details for Web of Science ID 000535265800016

    View details for PubMedID 32156780

  • Targeted Delivery of CXCL9 and OX40L by Mesenchymal Stem Cells Elicits Potent Antitumor Immunity MOLECULAR THERAPY Yin, P., Gui, L., Wang, C., Yan, J., Liu, M., Ji, L., Wang, Y., Ma, B., Gao, W. 2020; 28 (12): 2553-2563

    Abstract

    Major obstacles in immunotherapies include toxicities associated with systemic administration of therapeutic agents, as well as low tumor lymphocyte infiltration that hampers the efficacies. In this study, we report a mesenchymal stem cell (MSC)-based immunotherapeutic strategy in which MSCs specifically deliver T/natural killer (NK) cell-targeting chemokine CXCL9 and immunostimulatory factor OX40 ligand (OX40L)/tumor necrosis factor superfamily member 4 (TNFSF4) to tumor sites in syngeneic subcutaneous and azoxymethane (AOM)/dextran sulfate sodium (DSS)-induced spontaneous colon cancer mouse models. This approach generated potent local antitumor immunity by increasing the ratios of tumor-infiltrating CD8+ T and NK cells and production of antitumor cytokines and cytolytic proteins in the tumor microenvironment. Moreover, it improved the efficacy of programmed death-1 (PD-1) blockade in a syngeneic mouse model and significantly suppressed the growth of major histocompatibility complex class I (MHC class I)-deficient tumors. Our MSC-based immunotherapeutic strategy simultaneously recruits and activates immune effector cells at the tumor site, thus overcoming the problems with toxicities of systemic therapeutic agents and low lymphocyte infiltration of solid tumors.

    View details for DOI 10.1016/j.ymthe.2020.08.005

    View details for Web of Science ID 000596644000006

    View details for PubMedID 32827461

    View details for PubMedCentralID PMC7704751

  • beta-Catenin inhibition shapes tumor immunity and synergizes with immunotherapy in colorectal cancer ONCOIMMUNOLOGY Wang, C., Yan, J., Yin, P., Gui, L., Ji, L., Ma, B., Gao, W. 2020; 9 (1): 1809947

    Abstract

    In colorectal cancer, Wnt/β-catenin signaling is often aberrantly activated and associated with a T-cell-excluded phenotype which is a major obstacle for many immunotherapies. However, the effects of Wnt/β-catenin inhibition on tumor immunity and immunotherapy remain to be elucidated. In syngeneic mouse models of colorectal cancer, β-catenin/TCF inhibitor iCRT14 potently enhanced the infiltration of T and NK cells, without influencing their proliferation or the infiltration of most myeloid populations. Mechanistically, β-catenin inhibition upregulated while its overexpression suppressed the expression of T/NK cell-recruiting CXCR3 chemokines CXCL9/10/11 in both mouse and human colorectal cancer cells. Furthermore, iCRT14 treatment synergized with tumor vaccines or Treg cell ablation to achieve a complete inhibition of tumor growth in syngeneic models of CT26-OVA and MC38-S33Y.β-cat, respectively. Taken together, our work reveals that β-catenin inhibition shifts colorectal tumor microenvironment into a T-cell-inflamed phenotype and potentiates the efficacy of other immunotherapeutic strategies for colorectal cancer.

    View details for DOI 10.1080/2162402X.2020.1809947

    View details for Web of Science ID 000567155800001

    View details for PubMedID 32939327

    View details for PubMedCentralID PMC7470182