human
The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
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    INPUT: Glioblastoma multiforme is the most aggressive primary brain tumor in adults . Overexpression of the EGF receptor ( EGFR ) is recognized as a widespread oncogenic signature in glioblastoma multiforme , but the complexity of its contributions is not fully understood , nor the most effective ways to leverage anti-EGFR therapy in this setting . Hypoxia is known to drive the aggressive character of glioblastoma multiforme by promoting aerobic glycolysis rather than pyruvate oxidation carried out in mitochondria ( OXPHOS ) , a phenomenon termed the Warburg effect , which is a general feature of oncogenesis . In this study , we report that hypoxia drives expression of the pyruvate dehydrogenase kinase ( PDK1 ) and EGFR along with the hypoxia-inducing factor ( HIF)-1α in human glioblastoma multiforme cells . PDK1 is a HIF-1-regulated gene and our findings indicated that hypoxia-induced PDK1 expression may promote EGFR activation , initiating a feed-forward loop that can sustain malignant progression . RNAi-mediated attenuation of PDK1 and EGFR lowered PDK1-EGFR activation and decreased HIF-1α expression , shifting the Warburg phenotype to OXPHOS and inhibiting glioblastoma multiforme growth and proliferation . In clinical specimens of glioblastoma multiforme , we found that immunohistochemical expression of PDK1 , EGFR , and HIF-1α were elevated in glioblastoma multiforme specimens when compared with normal brain tissues . Collectively , our studies establish PDK1 as a key driver and candidate therapeutic target in glioblastoma multiforme .
    OUTPUT:

agent
sustaining proliferative signaling;cellular energetics
The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
    ###
    INPUT: Glioblastoma multiforme is the most aggressive primary brain tumor in adults . Overexpression of the EGF receptor ( EGFR ) is recognized as a widespread oncogenic signature in glioblastoma multiforme , but the complexity of its contributions is not fully understood , nor the most effective ways to leverage anti-EGFR therapy in this setting . Hypoxia is known to drive the aggressive character of glioblastoma multiforme by promoting aerobic glycolysis rather than pyruvate oxidation carried out in mitochondria ( OXPHOS ) , a phenomenon termed the Warburg effect , which is a general feature of oncogenesis . In this study , we report that hypoxia drives expression of the pyruvate dehydrogenase kinase ( PDK1 ) and EGFR along with the hypoxia-inducing factor ( HIF)-1α in human glioblastoma multiforme cells . PDK1 is a HIF-1-regulated gene and our findings indicated that hypoxia-induced PDK1 expression may promote EGFR activation , initiating a feed-forward loop that can sustain malignant progression . RNAi-mediated attenuation of PDK1 and EGFR lowered PDK1-EGFR activation and decreased HIF-1α expression , shifting the Warburg phenotype to OXPHOS and inhibiting glioblastoma multiforme growth and proliferation . In clinical specimens of glioblastoma multiforme , we found that immunohistochemical expression of PDK1 , EGFR , and HIF-1α were elevated in glioblastoma multiforme specimens when compared with normal brain tissues . Collectively , our studies establish PDK1 as a key driver and candidate therapeutic target in glioblastoma multiforme .
    OUTPUT:
