{"title":"Analysis of the Cancer Genome Atlas Data to Determine the Prognostic Value of GABPB1L and TERT in Glioblastoma","authors":"Jongwan Kim, Soo-Jung Jung, Jae-Ho Lee","doi":"10.46308/kmj.2021.00171","DOIUrl":null,"url":null,"abstract":"Glioblastoma multiforme (GBM) is the most lethal type in primary brain tumors, with most patients dying within one year after initial diagnosis. Its treatment as surgery with radiotherapy and chemotherapy has induced 2 and 5 years survival rates of 25 and 10%, respectively [1]. Moreover, clinical trials have validated only limited benefits of targeted regimens, because of invasive nature and low proliferative activity of GBM [2]. Transcription factors have chief roles in the regulation of cell development and maintenance; they are essential for cell maintenance, proliferation and apoptosis [3]. In these factors, GA-binding protein A forms a heterotetramer complex with its partner GA Binding Protein Transcription Factor Subunit Beta (GABPB) 1 or GABPB2; GABPB1 gene encodes the GABPB1 with its isoforms GABPB1-longer (GABPB1L) and GABPB1-shorter as the products of a different mRNA splicing. Similar to many other E-twenty-six (ETS) factors, they also had oncogenic activities and were associated with the pathogenesis of leukemia, prostate cancer, and other malignancies [4-6]. Recent study introduced novel role of GABPB1L and telomerase reverse transcriptase (TERT) in GBM [7]. When combined with temozolomide chemotherapy, inducible GABPB1L knockdown and the associated TERT reduction led to an impaired DNA damage response that resulted in profoundly reduced growth of GBM tumor in pISSN 2092-8335 · eISSN 2733-5380 Keimyung Med J 2021[Epub ahead of print] https://doi.org/10.46308/kmj.2021.00171 Original Article","PeriodicalId":166951,"journal":{"name":"Keimyung Medical Journal","volume":"13 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Keimyung Medical Journal","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.46308/kmj.2021.00171","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 1
Abstract
Glioblastoma multiforme (GBM) is the most lethal type in primary brain tumors, with most patients dying within one year after initial diagnosis. Its treatment as surgery with radiotherapy and chemotherapy has induced 2 and 5 years survival rates of 25 and 10%, respectively [1]. Moreover, clinical trials have validated only limited benefits of targeted regimens, because of invasive nature and low proliferative activity of GBM [2]. Transcription factors have chief roles in the regulation of cell development and maintenance; they are essential for cell maintenance, proliferation and apoptosis [3]. In these factors, GA-binding protein A forms a heterotetramer complex with its partner GA Binding Protein Transcription Factor Subunit Beta (GABPB) 1 or GABPB2; GABPB1 gene encodes the GABPB1 with its isoforms GABPB1-longer (GABPB1L) and GABPB1-shorter as the products of a different mRNA splicing. Similar to many other E-twenty-six (ETS) factors, they also had oncogenic activities and were associated with the pathogenesis of leukemia, prostate cancer, and other malignancies [4-6]. Recent study introduced novel role of GABPB1L and telomerase reverse transcriptase (TERT) in GBM [7]. When combined with temozolomide chemotherapy, inducible GABPB1L knockdown and the associated TERT reduction led to an impaired DNA damage response that resulted in profoundly reduced growth of GBM tumor in pISSN 2092-8335 · eISSN 2733-5380 Keimyung Med J 2021[Epub ahead of print] https://doi.org/10.46308/kmj.2021.00171 Original Article