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- 저자 : ( Winward Choy ) (검색결과 2 건)
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( Winward Choy ),( Carlito Lagman ),( Seung J. Lee ),( Timothy T. Bui ),( Michael Safaee ),( Isaac Yang ) 대한뇌종양학회 대한신경종양학회 2016 Brain Tumor Research and Treatment Vol.4 No.2
Background Improvement in antiviral therapies have been accompanied by an increased frequency of non-Acquired Immune Deficiency Syndrome (AIDS) defining malignancies, such as glioblastoma mul tiforme. Here, we investigated all reported cases of human immunodeficiency virus (HIV)-positive pa tients with glioblastoma and evaluated their clinical outcomes. A comprehensive review of the molecular pathogenetic mechanisms underlying glioblastoma development in the setting of HIV/AIDS is provided. Methods We performed a PubMed search using keywords “HIV glioma” AND “glioblastoma,” and “AIDS glioma” AND “glioblastoma.” Case reports and series describing HIV-positive patients with glioblastoma (histologically-proven World Health Organization grade IV astrocytoma) and reporting on HAART treatment status, clinical follow-up, and overall survival (OS), were included for the purposes of quantitative synthesis. Patients without clinical follow-up data or OS were excluded. Remaining articles were assessed for data extraction eligibility. Results A total of 17 patients met our inclusion criteria. Of these patients, 14 (82.4%) were male and 3 (17.6%) were female, with a mean age of 39.5±9.2 years (range 19-60 years). Average CD4 count at diagnosis of glioblastoma was 358.9±193.4 cells/mm3. Tumor progression rather than AIDS-associated complications dictated patient survival. There was a trend towards increased median survival with HAART treatment (12.0 vs 7.5 months, p=0.10) Conclusion Our data suggests that HAART is associated with improved survival in patients with HIV-associated glioblastoma, although the precise mechanisms underlying this improvement remain unclear.
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Winward Choy,Carlito Lagman,Seung J. Lee,Timothy T. Bui,Michael Safaee,Isaac Yang 대한뇌종양학회 2016 Brain Tumor Research and Treatment Vol. No.
Background Improvement in antiviral therapies have been accompanied by an increased frequency of non-Acquired Immune Deficiency Syndrome (AIDS) defining malignancies, such as glioblastoma multiforme. Here, we investigated all reported cases of human immunodeficiency virus (HIV)-positive patients with glioblastoma and evaluated their clinical outcomes. A comprehensive review of the molecular pathogenetic mechanisms underlying glioblastoma development in the setting of HIV/AIDS is provided. Methods We performed a PubMed search using keywords “HIV glioma” AND “glioblastoma,” and “AIDS glioma” AND “glioblastoma.” Case reports and series describing HIV-positive patients with glioblastoma (histologically-proven World Health Organization grade IV astrocytoma) and reporting on HAART treatment status, clinical follow-up, and overall survival (OS), were included for the purposes of quantitative synthesis. Patients without clinical follow-up data or OS were excluded. Remaining articles were assessed for data extraction eligibility. Results A total of 17 patients met our inclusion criteria. Of these patients, 14 (82.4%) were male and 3 (17.6%) were female, with a mean age of 39.5±9.2 years (range 19–60 years). Average CD4 count at diagnosis of glioblastoma was 358.9±193.4 cells/mm3. Tumor progression rather than AIDS-associated complications dictated patient survival. There was a trend towards increased median survival with HAART treatment (12.0 vs 7.5 months, p=0.10) Conclusion Our data suggests that HAART is associated with improved survival in patients with HIV-associated glioblastoma, although the precise mechanisms underlying this improvement remain unclear.
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