[대학원 생명과학과 세미나 안내] 

연사 : 윤경완 교수 (호서대학교 생명공학과)

연제 : New strategies for improving current cancer immunotherapy: Novel immune checkpoint blockade and microbiome modulation 

일시 : 2019년 11월 25일 (월) 오후 5시 

장소 : 하나과학관 A동 109호

초청교수 : 최의주 교수

Abstract

Immunotherapy is a promising treatment strategy for cancer that has recently shown unprecedented survival benefits in selected patients. A number of immunomodulatory agents that target immune system checkpoints such as the cytotoxic T-lymphocyte antigen 4 (CTLA-4), the programmed death-1 (PD-1) or its ligand (PD-L1), have approved for the treatment of multiple cancers including malignant melanoma, non-small cell lung cancer, renal cell carcinoma, classical Hodgkin lymphoma, and recurrent or metastatic head and neck squamous cell carcinoma. Although immune checkpoint blockade therapy elicits durable antitumor effects in multiple cancers, high rates of resistance still limit anti-tumor efficacy of immune checkpoint blockade therapy. Therefore, understanding resistant mechanism against immune checkpoint blockade therapy, biomarker- based prediction of anti-tumor efficacy in patients, and improvement of current therapeutic efficacy by combination with enhancing materials is currently most highlighted in cancer research area. Here, novel immune checkpoint proteins will be introduced as combinational therapeutic targets of PD-1 blockade therapy. Based on evaluation of novel immune checkpoint protein expression in multiple cancer patient cohorts, druggable potential of novel immune checkpoint targets in specific types of cancer will be addressed. As a different way of approach to investigate enhancing PD-1 blockade therapy, microbiome of cancer patients or normal people was analyzed by metagenome sequencing. Several specific beneficial microbes were identified and proved to enhance PD-1 blockade therapy in preclinical model. Multi-omic studies using metagenomic, genomic, transcriptomic and metabolomic analysis revealed that the immune-stimulating molecules of beneficial microbes contribute to enhancing PD-1 blockade therapy.