EXPERTISE

頭頸部腫瘤分子醫學, 腫瘤病毒致癌機轉, 蛋白質酪胺酸激酶, 基因融合

RESEARCH INTERESTS

Head and neck cancers, including oral cancer and nasopharyngeal carcinoma (NPC), are caused by known extrinsic factors and develop within pre-neoplastic fields of genetically or epigenetically altered cells. In Taiwan, betel quid chewing in oral cancer and Epstein-Barr virus (EBV) infection in NPC are thought to be unique etiologies that promote tumor progression. My lab has been directed our efforts on two main projects:

1. To identify overexpressed protein tyrosine kinases in oral caner cells.
2. To elucidate the role of EBV lytic cycle replication in NPC pathogenesis.

For the first project we hypothesized that by knowing what protein tyrosine kinases that drive oral cancer cell survive, would provide rational molecularly targeted therapies for oral cancer. For the second project we specifically asked what are the host factors that restrict EBV lytic cycle replication in nasopharyngeal cells.

RESEARCH ACTIVITIES & ACCOMPLISHMENT

Accumulating evidence indicates that the tumor microenvironment (TME) of head and neck cancer is very immunosuppressive. Researchers in immuno-oncology field published convincing examples by implanting patient derived xenograft (PDX) in CD34+ hematopoietic stem cells reconstituted NOG/NSG mice, termed huMice, to recapitulate HNC TME. As a step to establish similar models in the lab, in collaboration with Hsu SC at NIIDV, NHRI, we successfully constructed a pair of oral squamous cell carcinoma (OSCC) TW2.6 cell bearing-NOG and -huMice animal models. Preliminary results indicated that OSCC cells implanted in huMice recruited CD68+ and CD3+ human immune cells and expressed immunosuppressors, IDO1 and PD-L1.

In parallel, by using in silico tools e.g. CIBERSORT and alike, we were able to portrait tumor infiltrating lymphocytes (TILs) in the NCKU 40 OSCC tumor/adjacent normal paired tissues. Integrated analysis of RNA-seq data, immunohistochemical staining, and flow cytometer analysis are in progress.