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: Aerobic glycolysis and mitochondrial dysfunction are common features of aggressive cancer growth . We observed promoter methylation and loss of expression in neurofilament heavy polypeptide ( NEFH ) in a significant proportion of primary esophageal squamous cell carcinoma ( ESCC ) samples that were of a high tumor grade and advanced stage . RNA interference-mediated knockdown of NEFH accelerated ESCC cell growth in culture and increased tumorigenicity in vivo , whereas forced expression of NEFH significantly inhibited cell growth and colony formation . Loss of NEFH caused up-regulation of pyruvate kinase-M2 type and down-regulation of pyruvate dehydrogenase , via activation of the Akt/beta-catenin pathway , resulting in enhanced aerobic glycolysis and mitochondrial dysfunction . The acceleration of glycolysis and mitochondrial dysfunction in NEFH-knockdown cells was suppressed in the absence of beta-catenin expression , and was decreased by the treatment of 2-Deoxyglucose , a glycolytic inhibitor , or API-2 , an Akt inhibitor . Loss of NEFH activates the Akt/beta-catenin pathway and increases glycolysis and mitochondrial dysfunction . Cancer cells with methylated NEFH can be targeted for destruction with specific inhibitors of deregulated downstream pathways .
    OUTPUT:

agent
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.
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    INPUT: Aerobic glycolysis and mitochondrial dysfunction are common features of aggressive cancer growth . We observed promoter methylation and loss of expression in neurofilament heavy polypeptide ( NEFH ) in a significant proportion of primary esophageal squamous cell carcinoma ( ESCC ) samples that were of a high tumor grade and advanced stage . RNA interference-mediated knockdown of NEFH accelerated ESCC cell growth in culture and increased tumorigenicity in vivo , whereas forced expression of NEFH significantly inhibited cell growth and colony formation . Loss of NEFH caused up-regulation of pyruvate kinase-M2 type and down-regulation of pyruvate dehydrogenase , via activation of the Akt/beta-catenin pathway , resulting in enhanced aerobic glycolysis and mitochondrial dysfunction . The acceleration of glycolysis and mitochondrial dysfunction in NEFH-knockdown cells was suppressed in the absence of beta-catenin expression , and was decreased by the treatment of 2-Deoxyglucose , a glycolytic inhibitor , or API-2 , an Akt inhibitor . Loss of NEFH activates the Akt/beta-catenin pathway and increases glycolysis and mitochondrial dysfunction . Cancer cells with methylated NEFH can be targeted for destruction with specific inhibitors of deregulated downstream pathways .
    OUTPUT:
