Lianbao Kong
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Research Subjects
Lianbao Kong has a total of 179 co-authors. Here are the top co-authors by number of shared publications:
Deming Zhu
18 shared publications- Chengdian Rao
State Key Laboratory of Natural Medicines, Jiangsu Key Laboratory of Carcinogenesis and Intervention, Department of Physiology, School of Basic Medicine and Clinical Pharmacy, China Pharmaceutical University, Nanjing, China
15 shared publications - Chenxi Wang
State Key Laboratory of Natural Medicines, Jiangsu Key Laboratory of Carcinogenesis and Intervention, Department of Physiology, School of Basic Medicine and Clinical Pharmacy, China Pharmaceutical University, Nanjing, China
15 shared publications Jinyi Wang
Hepatobiliary Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu Province, China; Department of Hepatobiliary and Pancreatic Surgery, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, China; Key Laboratory of Liver Transplantation, Chinese Academy of Medical Sciences, National Health Commission (NHC) Key Laboratory of Hepatobiliary Cancers, Nanjing, Jiangsu Province, China
15 shared publications- Kai Zhao
State Key Laboratory of Natural Medicines, Jiangsu Key Laboratory of Carcinogenesis and Intervention, Department of Physiology, School of Basic Medicine and Clinical Pharmacy, China Pharmaceutical University, Nanjing, China
15 shared publications - Lulu Zhang
Department of Clinical Pharmacology, School of Pharmacy, Nanjing Medical University, Nanjing, China
15 shared publications
Latest Publications
- Open Access
- 15 September 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 10 from SEPTIN7 Enhances Tumorigenesis and Therapeutic Resistance in Hepatocellular Carcinoma by Promoting FGFR4 Stabilization and Recycling
A novel combination strategy co-targeting the USP7-FGFR4 axis and standard therapies for HCC.
- 15 September 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 10 from SEPTIN7 Enhances Tumorigenesis and Therapeutic Resistance in Hepatocellular Carcinoma by Promoting FGFR4 Stabilization and Recycling
A novel combination strategy co-targeting the USP7-FGFR4 axis and standard therapies for HCC.
- Open Access
- 15 September 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 2 from SEPTIN7 Enhances Tumorigenesis and Therapeutic Resistance in Hepatocellular Carcinoma by Promoting FGFR4 Stabilization and Recycling
SEPTIN7 enhances stemness features and confers resistance to standard therapy in HCC cells in vitro.
- 15 September 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 2 from SEPTIN7 Enhances Tumorigenesis and Therapeutic Resistance in Hepatocellular Carcinoma by Promoting FGFR4 Stabilization and Recycling
SEPTIN7 enhances stemness features and confers resistance to standard therapy in HCC cells in vitro.
- Open Access
- 15 September 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 3 from SEPTIN7 Enhances Tumorigenesis and Therapeutic Resistance in Hepatocellular Carcinoma by Promoting FGFR4 Stabilization and Recycling
SEPTIN7 enhances stemness features and confers resistance to standard therapy in HCC cells in vivo.
- 15 September 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 3 from SEPTIN7 Enhances Tumorigenesis and Therapeutic Resistance in Hepatocellular Carcinoma by Promoting FGFR4 Stabilization and Recycling
SEPTIN7 enhances stemness features and confers resistance to standard therapy in HCC cells in vivo.
- Open Access
- 15 September 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 4 from SEPTIN7 Enhances Tumorigenesis and Therapeutic Resistance in Hepatocellular Carcinoma by Promoting FGFR4 Stabilization and Recycling
SEPTIN7 potentiates tumorgenesis and drug resistance of HCC in both liver-specific SEPTIN7 knockout mice and patient-derived organoids.
- 15 September 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 4 from SEPTIN7 Enhances Tumorigenesis and Therapeutic Resistance in Hepatocellular Carcinoma by Promoting FGFR4 Stabilization and Recycling
SEPTIN7 potentiates tumorgenesis and drug resistance of HCC in both liver-specific SEPTIN7 knockout mice and patient-derived organoids.
- Open Access
- 15 September 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 6 from SEPTIN7 Enhances Tumorigenesis and Therapeutic Resistance in Hepatocellular Carcinoma by Promoting FGFR4 Stabilization and Recycling
SEPTIN7 inhibits K48-linked ubiquitin-mediated proteasomal degradation of FGFR4 by facilitating the recruitment of USP7.
- 15 September 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 6 from SEPTIN7 Enhances Tumorigenesis and Therapeutic Resistance in Hepatocellular Carcinoma by Promoting FGFR4 Stabilization and Recycling
SEPTIN7 inhibits K48-linked ubiquitin-mediated proteasomal degradation of FGFR4 by facilitating the recruitment of USP7.
- Open Access
- 15 September 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 5 from SEPTIN7 Enhances Tumorigenesis and Therapeutic Resistance in Hepatocellular Carcinoma by Promoting FGFR4 Stabilization and Recycling
SEPTIN7 promotes HCC stemness and therapeutic resistance by enhancing the stability and signaling activity of FGFR4.
- 15 September 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 5 from SEPTIN7 Enhances Tumorigenesis and Therapeutic Resistance in Hepatocellular Carcinoma by Promoting FGFR4 Stabilization and Recycling
SEPTIN7 promotes HCC stemness and therapeutic resistance by enhancing the stability and signaling activity of FGFR4.
- Open Access
- 15 September 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 8 from SEPTIN7 Enhances Tumorigenesis and Therapeutic Resistance in Hepatocellular Carcinoma by Promoting FGFR4 Stabilization and Recycling
SEPTIN7 promotes HCC stemness and therapeutic resistance via a RACK1-dependent mechanism, which facilitates FGFR4 phosphorylation at S440 site.
- 15 September 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 8 from SEPTIN7 Enhances Tumorigenesis and Therapeutic Resistance in Hepatocellular Carcinoma by Promoting FGFR4 Stabilization and Recycling
SEPTIN7 promotes HCC stemness and therapeutic resistance via a RACK1-dependent mechanism, which facilitates FGFR4 phosphorylation at S440 site.
- Open Access
- 15 September 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 7 from SEPTIN7 Enhances Tumorigenesis and Therapeutic Resistance in Hepatocellular Carcinoma by Promoting FGFR4 Stabilization and Recycling
RACK1 facilitates FGFR4 phosphorylation at S440 site.
- 15 September 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 7 from SEPTIN7 Enhances Tumorigenesis and Therapeutic Resistance in Hepatocellular Carcinoma by Promoting FGFR4 Stabilization and Recycling
RACK1 facilitates FGFR4 phosphorylation at S440 site.
- Open Access
- 15 September 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 9 from SEPTIN7 Enhances Tumorigenesis and Therapeutic Resistance in Hepatocellular Carcinoma by Promoting FGFR4 Stabilization and Recycling
A phosphorylation-dominant and ubiquitination-reinforced mechanism in SEPTIN7-mediated FGFR4 activity.
- 15 September 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 9 from SEPTIN7 Enhances Tumorigenesis and Therapeutic Resistance in Hepatocellular Carcinoma by Promoting FGFR4 Stabilization and Recycling
A phosphorylation-dominant and ubiquitination-reinforced mechanism in SEPTIN7-mediated FGFR4 activity.
- Open Access
- 15 September 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table 1 from SEPTIN7 Enhances Tumorigenesis and Therapeutic Resistance in Hepatocellular Carcinoma by Promoting FGFR4 Stabilization and Recycling
Supplementary Table 1 List of Abbreviations.
- 15 September 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 1 from SEPTIN7 Enhances Tumorigenesis and Therapeutic Resistance in Hepatocellular Carcinoma by Promoting FGFR4 Stabilization and Recycling
Supplementary Table 1 List of Abbreviations.