| Summary: | 碩士 === 臺北醫學大學 === 醫學科學研究所 === 97 === Giloma derive from glial cell, which contribute about 90% of brain cells. The functions of glial cells are offering support and nutrition, forming myelin sheath and blood brain barrier.The most common glioma is glioblastoma multiforme (GBM) and the possible causes are not fully understood. Neurosurgery unable to remove the glioma from normal brain clearly；Glioma even resisten to high dose of radiotherapy and chemotherapy. The prognosis of malignant glioma remains dismal and the estimated median survival time is <1 year.It is emergent to develop new therapic policy and find out target genes. Previous data investigate that cotreatment with interleukin-2 (IL-2) and histamine inhibits growth and angiogenesis in malignant glioma. It also suggests that histamine has function of tumor suppression. In cytosol, histamine is metabolized by histamine-N- methyltransferase (HNMT). The concentration of histamine and its products have association with glioma. However, there is no direct evidence to investigate the roles of HNMT in growth and pathogenesis of glioma. Our data demonstrate that either specisement of GBM or glioma cell lines express more HNMT than normal brain tissue. More amount of HNMT suggests less tumorspressive histamine. On the other hands, we also find that epidermal growth factor (EGF), a glioma inducing factor, increases the expression of HNMT and changes the location of HNMT in glioma cell line. Collectively, our data provide hint that HNMT is another noval theraptic target for deadly glioma.
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