Ji Hongbin

Biography

JI Hongbin is a Professor of Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, hanghai, China. Research Areas: lung cancer; metastasis; biomarkers; genomics; genetics; metabolism;oncogenes; tumor suppressors; mouse model; drug discovery; LKB1; EGF receptor kinase domain mutation; Research Interests: Lung cancer is one of the most devastating diseases worldwide with 5-year survival rate approximately 15%. The high mortality is mainly attributable to the poor understanding of the mechanisms involved in lung cancerigenesis. Our research interest is to decipher the molecular mechanisms involved in lung cancer initiation, malignant progression, transdifferentiation and metastasis, with a long-term goal to identify effective biomarkers for diagnosis and therapeutic targets for personalized medicine. In the past decade, we have mainly focused on: the identification of oncogenic drivers in lung cancer and the functional and mechanistic study of these important lung cancer related genes. In collaboration with Fudan University Shanghai Cancer Center, we have collected over 3000 human lung cancer specimens with comprehensive clinical information. Integrative genetic analyses of these lung cancer samples provides a spectrum of genomic DNA copy number variation, gene expression, gene mutation and gene fusions, which hopefully leads to the discovery to important oncogenic drivers in lung cancer. Among these candidates, LKB1 and the HPO pathway are proven to be important negative regulator of lung cancer malignant progression. We are actively investigating the potential function and mechanism of these molecules and seeking a way to treat these lung cancer with the inactivation of LKB1 or HPO pathway. Currently, we are also very interested in lung cancer plasticity and drug resistance. Lung cancer is notorious its strong plasticity, which provides the major force for driving malignant progression, metastasis and more importantly, the therapeutic failure. EGFR-targeted therapy has been proved as a gigantic success in lung cancer clinic. However, it only lasts for half a year or so and all the patients inevitably relapse with progressive disease. Molecular reprogramming and phenotypic transition to small cell lung carcinoma have been reported responsible for cancer cells to escape drug treatment. Our recent findings of the transdifferentiation of lung adenocarcinoma to squamous cell carcinoma also suggest that the phenotypic transition represents a novel mechanism of lung cancer drug resistance. Understanding cancer plasticity during malignant progression and drug resistance hopefully provides a way for clinical management of this deadly disease. We take advantage of both genetically engineered mouse model (GEMM) and patient-derived xenograft (PDX) model to investigate the link between tumor plasticity and drug resistance. Hopefully, these works will provide a better understanding of lung cancerigenesis and improve current strategies for clinical lung cancer treatment.

Research Interest

Lung cancer is one of the most devastating diseases worldwide with 5-year survival rate approximately 15%. The high mortality is mainly attributable to the poor understanding of the mechanisms involved in lung cancerigenesis. Our research interest is to decipher the molecular mechanisms involved in lung cancer initiation, malignant progression, transdifferentiation and metastasis, with a long-term goal to identify effective biomarkers for diagnosis and therapeutic targets for personalized medicine. In the past decade, we have mainly focused on: the identification of oncogenic drivers in lung cancer and the functional and mechanistic study of these important lung cancer related genes. In collaboration with Fudan University Shanghai Cancer Center, we have collected over 3000 human lung cancer specimens with comprehensive clinical information. Integrative genetic analyses of these lung cancer samples provides a spectrum of genomic DNA copy number variation, gene expression, gene mutation and gene fusions, which hopefully leads to the discovery to important oncogenic drivers in lung cancer. Among these candidates, LKB1 and the HPO pathway are proven to be important negative regulator of lung cancer malignant progression. We are actively investigating the potential function and mechanism of these molecules and seeking a way to treat these lung cancer with the inactivation of LKB1 or HPO pathway. Currently, we are also very interested in lung cancer plasticity and drug resistance. Lung cancer is notorious its strong plasticity, which provides the major force for driving malignant progression, metastasis and more importantly, the therapeutic failure. EGFR-targeted therapy has been proved as a gigantic success in lung cancer clinic. However, it only lasts for half a year or so and all the patients inevitably relapse with progressive disease. Molecular reprogramming and phenotypic transition to small cell lung carcinoma have been reported responsible for cancer cells to escape drug treatment. Our recent findings of the transdifferentiation of lung adenocarcinoma to squamous cell carcinoma also suggest that the phenotypic transition represents a novel mechanism of lung cancer drug resistance. Understanding cancer plasticity during malignant progression and drug resistance hopefully provides a way for clinical management of this deadly disease. We take advantage of both genetically engineered mouse model (GEMM) and patient-derived xenograft (PDX) model to investigate the link between tumor plasticity and drug resistance. Hopefully, these works will provide a better understanding of lung cancerigenesis and improve current strategies for clinical lung cancer treatment.