由 sufang 在 四, 08/21/2014 – 09:57 發表 Pre-published Temp
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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 have been directed our efforts on two main projects:
- To identify overexpressed protein tyrosine kinases (PTKs) in oral caner cells.
- 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 (PTKs) 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.
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Research Activities & Accomplishment
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- Role of collagen receptor DDR1 in oral cancer pathogenesis:
- DDR1-mediated cell survival
- DDR1-mediated collective cancer cell migration
- FGFR3 gene fusions in head and neck cancer:
- Prevalence of FGFR3-TACC3 gene fusion in oral cancer
- Oncogenic role of FGFR3-TACC3 gene fusion in oral cancer cells
- EBV Rta interferes with CTCF binding in both host and viral genomes:
- Rta expression enhances DNA methylation in cellular CpG islands
- Rta expression disrupts the bindings of CTCF in EBV genome
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舊貨不刪:
- Dr. Lin’s laboratory is directed at understanding the reactivation mechanism of two human herpesviruses: Epstein-Barr virus (EBV) and Kaposi’s sarcoma associated herpesvirus (KSHV). During their infections, the conversion of an EBV or KSHV latent genome into a lytic replicating one is defined as reactivation. In single-gene systems, several EBV and KSHV encoded latent proteins are oncogenic, indicating that these latent proteins are crucial to EBV and KSHV pathogenesis. Recently, emerging evidence indicates that repeated lytic reactivation may also play a role in EBV and KSHV tumorigenesis. To delineate the molecular processes of EBV and KSHV lytic reactivations, we established a doxycycline inducible system in HEK293 cells that produces a nearly permissive replication phenotype for both EBV and KSHV. Because this system is homogeneous and robust, it is now feasible to elucidate host and viral factors that contribute to regulate the EBV and KSHV reactivations. For more details, please visit Here.
- Dr. Lin’s second research interest is focused on identifying oncogenic protein tyrosine kinases (PTK) that are involved in oral cancers. Precise molecular classification of cancer subtypes coupled with target inhibition of altered PTK activity has been clinically proven in chronic myelogenous leukemia (ABL), gastrointestinal stromal tumors (c-KIT), ERBB2 positive breast cancer (ERBB2), and a portion of advanced non-small-cell lung cancer (mutated EGFR). A prerequisite to the success of these role models is to precisely uncover the dys-regulated or activated PTK in the cancer cells. To this end, Dr. Lin’s lab has recently identified four PTKs over-expressed in Taiwanese oral squamous cell carcinoma cells. There pathologic relevance in oral cancer progression are under investigations. For more details, please explore Here.
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Research Activities & Accomplishment
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- Overexpression of DDR1 in oral cancer cells
- Protein phosphorylation of KSHV RTA/ORF50 is involved in KSHV lytic reactivation
- Suppressive regulation of KSHV RTA/ORF50 with O-GlcNAcylation
- Roles of OSCC-specific PTKs in oral cancer pathogenesis
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