Biao Yang
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Biao Yang has a total of 16 co-authors. Here are the top co-authors by number of shared publications:
- Bi-Sen Ding
Key Laboratory of Birth Defects and Related Diseases of Women and Children of MOE, State Key Laboratory of Biotherapy, West China Second University Hospital, Sichuan University, Chengdu, China
2 shared publications Qiaoqi Li
Abdominal Oncology Ward, Division of Medical Oncology, Cancer Center, West China Hospital, Sichuan University
2 shared publications- Zhongwei Cao
Key Lab of Birth Defects and Related Diseases of Women and Children of MOE, State Key Lab of Biotherapy, State Key Laboratory of Respiratory Health and Multimorbidity, West China School of Basic Medical Sciences & Forensic Medicine, West China Second University Hospital, Sichuan University, Chengdu, China
2 shared publications Cheng Yi
Division of Abdominal Tumor Multimodality Treatment, Cancer Center, West China Hospital, Sichuan University, Chengdu, China
1 shared publicationHanjun Mo
Division of Abdominal Tumor Multimodality Treatment, Cancer Center, West China Hospital, Sichuan University, Chengdu, China
1 shared publication- Hong Zhu
Department of Medical Oncology, Cancer Center, West China Hospital, Sichuan University, Chengdu, China
1 shared publication
Latest Publications
- 2 July 2026
- Published by Elsevier in Cell Stem Cell
- Vol. 33 (7) , 1057-1059
Long-term lessons from MATCH01 macrophage therapy in cirrhosis
- 2 July 2026
- Published by Elsevier in Cell Stem Cell
- Vol. 33 (7) , 1057-1059
Long-term lessons from MATCH01 macrophage therapy in cirrhosis
- Open Access
- 12 May 2026
- Published by Frontiers Media SA in Frontiers in Immunology
- Vol. 17, 1790214
Stress accelerates hepatocellular carcinoma progression via a gut microbial-metabolite axis
Background: Hepatocellular carcinoma ranks among the most prevalent malignancies worldwide. While stress can modulate tumor initiation, progression, metastasis, and therapeutic response through diverse mechanisms, its specific role in hepatocellular carcinoma pathobiology remains elusive. This study aimed to elucidate the role of the gut microbiota in stress-promoted hepatocellular carcinoma progression and to uncover the pathways associated with disease progression. Methods: Integrating clinical and preclinical models, we delineated stress-induced restructuring of the gut microbiota and functionally restored specific microbial constituents. Mechanistic insights into the microbial metabolite indole-3-propionic acid were derived through in vitro and in vivo interrogations of the hepatocellular carcinoma tumor microenvironment. Results: Stress profoundly remodels the gut microbiota, with Phocaeicola vulgatus being significantly reduced. Restoration of Phocaeicola vulgatus or administration of its tryptophan-derived metabolite indole-3-propionic acid significantly attenuated hepatocellular carcinoma progression in vivo . Indole-3-propionic acid treatment reduced endothelial JAM2 expression and was associated with reduced JAM2–F11R-mediated endothelial–macrophage crosstalk in hepatocellular carcinoma, which may contribute to suppression of tumor progression. Conclusions: These findings support a role for the stress–gut microbiota–metabolite–tumor microenvironment axis in hepatocellular carcinoma progression and suggest potential translational targets for microbiome-based therapeutic strategies.
- 12 May 2026
- Published by Frontiers Media SA in Frontiers in Immunology
- Vol. 17, 1790214
Open AccessStress accelerates hepatocellular carcinoma progression via a gut microbial-metabolite axis
Background: Hepatocellular carcinoma ranks among the most prevalent malignancies worldwide. While stress can modulate tumor initiation, progression, metastasis, and therapeutic response through diverse mechanisms, its specific role in hepatocellular carcinoma pathobiology remains elusive. This study aimed to elucidate the role of the gut microbiota in stress-promoted hepatocellular carcinoma progression and to uncover the pathways associated with disease progression. Methods: Integrating clinical and preclinical models, we delineated stress-induced restructuring of the gut microbiota and functionally restored specific microbial constituents. Mechanistic insights into the microbial metabolite indole-3-propionic acid were derived through in vitro and in vivo interrogations of the hepatocellular carcinoma tumor microenvironment. Results: Stress profoundly remodels the gut microbiota, with Phocaeicola vulgatus being significantly reduced. Restoration of Phocaeicola vulgatus or administration of its tryptophan-derived metabolite indole-3-propionic acid significantly attenuated hepatocellular carcinoma progression in vivo . Indole-3-propionic acid treatment reduced endothelial JAM2 expression and was associated with reduced JAM2–F11R-mediated endothelial–macrophage crosstalk in hepatocellular carcinoma, which may contribute to suppression of tumor progression. Conclusions: These findings support a role for the stress–gut microbiota–metabolite–tumor microenvironment axis in hepatocellular carcinoma progression and suggest potential translational targets for microbiome-based therapeutic strategies.
- Open Access
- 1 July 2025
- Published by AME Publishing Company in Quantitative Imaging in Medicine and Surgery
- Vol. 15 (7) , 6578-6583
Transarterial chemoembolization for inoperable primary cardiac angiosarcoma: a description of two cases and literature analysis
Transarterial chemoembolization for inoperable primary cardiac angiosarcoma: a description of two cases and literature analysis
- 1 July 2025
- Published by AME Publishing Company in Quantitative Imaging in Medicine and Surgery
- Vol. 15 (7) , 6578-6583
Open AccessTransarterial chemoembolization for inoperable primary cardiac angiosarcoma: a description of two cases and literature analysis
Transarterial chemoembolization for inoperable primary cardiac angiosarcoma: a description of two cases and literature analysis
- Open Access
- 24 September 2022
- Published by MDPI AG in Pharmaceutics
- Vol. 14 (10) , 2033
Nanoparticle-Based Therapeutic Strategies for Enhanced Pancreatic Ductal Adenocarcinoma Immunotherapy
Immunotherapy has dramatically changed prognosis for patients with malignant tumors. However, as a non-immunogenic tumor, pancreatic ductal adenocarcinoma (PDAC) has a low response to immunotherapy. Factors that contribute to the inefficiency of PDAC immunotherapy include the tumor microenvironment (TME) and its dense stroma, which acts as a barrier for drug delivery and immune cell infiltration. Recent studies have shown that nanoparticle-based therapeutic strategies have more promising applications in improving drug delivery and reversing the immunosuppressive TME for PDAC. Therefore, nanomaterial-based therapeutic approaches are expected to enhance the effectiveness of immunotherapy and improve prognosis of patients with PDAC. Here, we outline the status and dilemma of PDAC immunotherapy, and summarize the latest advances in nanoparticle-based treatment strategies to enhance the efficacy of PDAC immunotherapy.
- 24 September 2022
- Published by MDPI AG in Pharmaceutics
- Vol. 14 (10) , 2033
Open AccessNanoparticle-Based Therapeutic Strategies for Enhanced Pancreatic Ductal Adenocarcinoma Immunotherapy
Immunotherapy has dramatically changed prognosis for patients with malignant tumors. However, as a non-immunogenic tumor, pancreatic ductal adenocarcinoma (PDAC) has a low response to immunotherapy. Factors that contribute to the inefficiency of PDAC immunotherapy include the tumor microenvironment (TME) and its dense stroma, which acts as a barrier for drug delivery and immune cell infiltration. Recent studies have shown that nanoparticle-based therapeutic strategies have more promising applications in improving drug delivery and reversing the immunosuppressive TME for PDAC. Therefore, nanomaterial-based therapeutic approaches are expected to enhance the effectiveness of immunotherapy and improve prognosis of patients with PDAC. Here, we outline the status and dilemma of PDAC immunotherapy, and summarize the latest advances in nanoparticle-based treatment strategies to enhance the efficacy of PDAC immunotherapy.