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    <responseDate>2026-10-12T18:48:33Z</responseDate>
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    <identifier>10.57760/sciencedb.37016</identifier>
    <datestamp>2026-02-10T18:05:56Z</datestamp>
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<oai_dc:dc xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
  <dc:date>2026-02-10</dc:date>
  <dc:title>Integrated multi omics analysis reveals AFAP1L1 as a prognostic indicator and immune related therapeutic target in glioma</dc:title>
  <dc:identifier>doi:10.57760/sciencedb.37016</dc:identifier>
  <dc:language>en</dc:language>
  <dc:description>Methods: Clinical and transcriptomic data from glioma patients were downloaded from The Cancer Gene Atlas (TCGA), Chinese Glioma Genome Atlas (CGGA), and GSE117891 to explore the association between AFAP1L1 expression and glioma prognosis, somatic mutations, immune cell infiltration and enrichment pathway within glioma. Western blotting and real-time polymerase chain reaction (PCR) detected AFAP1L1 messenger RNA (mRNA) and protein expression in glioma patients. Results: We found patients with high AFAP1L1 expression tended to have a worse prognosis, and AFAP1L1 was identified as an independent risk factor. Furthermore, glioma patients with high AFAP1L1 expression exhibited lower levels of somatic mutations, with amplification of oncogenes such as epidermal growth factor receptor and deletion of tumor suppressor genes like Cyclin-Dependent Kinase Inhibitor 2A(CDKN2A[SL1]&amp;nbsp;). Analysis using the estimate algorithm revealed a positive correlation between AFAP1L1 and the immune microenvironment. Tide analysis indicated that glioma patients with high AFAP1L1 expression had poorer response to immune therapy. Single cell analysis illustrated that AFAP1L1 expression was mainly concentrated in glioma cells. Enrichment analysis indicated a potential association between AFAP1L1 and the small Cyclin-Dependent Kinase Inhibitor 2A(GTPases[SL2]&amp;nbsp;), Hypoxia-Inducible Factor 1(HIF-1[SL3]&amp;nbsp;), focal adhesion and Mitogen-Activated Protein Kinase(MAPK) [SL4]&amp;nbsp;signaling pathways.  需要补充英文全称需要补充英文全称&amp;nbsp;需要补充英文全称&amp;nbsp;需要补充英文全称&amp;nbsp;</dc:description>
  <dc:subject>low-grade gliomas; glioblastoma; actin filament-associated protein 1; immune microenvironment; single cell RNA sequencing</dc:subject>
  <dc:creator>李岱</dc:creator>
  <dc:creator>王安美</dc:creator>
  <dc:creator>魏成龙</dc:creator>
  <dc:rights>PUBLIC</dc:rights>
  <dc:rights>https://creativecommons.org/licenses/by-nc/4.0/</dc:rights>
  <dc:type>dataset</dc:type>
  <dc:publisher>Science Data Bank</dc:publisher>
</oai_dc:dc>

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