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: Inflammation which is an indispensable participant in tumor progression is intricately linked with redox modulation . The pro-inflammatory cytokine Tumor Necrosis Factor ( TNFalpha ) elevates reactive oxygen species ( ROS ) in glioblastoma multiforme ( GBM ) . As both TNFalpha and oxidative stress independently play role in regulating cytoskeletal organization and cell survival pathways we investigated whether TNFalpha mediated oxidative stress regulates responses that offer survival advantages to glioblastoma cells . Treatment with TNFalpha elevated Akt phosphorylation in glioma cells . Increased in Akt phosphorylation was concurrent with the decrease in ROS scavenger SOD-1 levels . TNFalpha mediated increase in Akt phosphorylation was dependent on oxidative stress as Akt phosphorylation was abrogated in the presence of ROS inhibitor and elevated in cells transfected with SOD-1 siRNA . TNFalpha altered actin cytoskeletal organization and increased Cdc42 levels . This increase in Cdc42 was concomitant with its increased interaction with scaffold protein IQGAP-1 . Also , we report for the first time a ROS dependent interaction between pAkt and IQGAP-1 in TNFalpha treated cells . Importantly , Akt inhibition not only reversed TNFalpha mediated changes in actin cytoskeletal organization but also abrogated anchorage independent growth . Together , these results suggest that TNFalpha induced oxidative stress affects Akt activation to regulate actin organization and growth of glioma cells .
    OUTPUT:

agent
tumor promoting inflammation
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: Inflammation which is an indispensable participant in tumor progression is intricately linked with redox modulation . The pro-inflammatory cytokine Tumor Necrosis Factor ( TNFalpha ) elevates reactive oxygen species ( ROS ) in glioblastoma multiforme ( GBM ) . As both TNFalpha and oxidative stress independently play role in regulating cytoskeletal organization and cell survival pathways we investigated whether TNFalpha mediated oxidative stress regulates responses that offer survival advantages to glioblastoma cells . Treatment with TNFalpha elevated Akt phosphorylation in glioma cells . Increased in Akt phosphorylation was concurrent with the decrease in ROS scavenger SOD-1 levels . TNFalpha mediated increase in Akt phosphorylation was dependent on oxidative stress as Akt phosphorylation was abrogated in the presence of ROS inhibitor and elevated in cells transfected with SOD-1 siRNA . TNFalpha altered actin cytoskeletal organization and increased Cdc42 levels . This increase in Cdc42 was concomitant with its increased interaction with scaffold protein IQGAP-1 . Also , we report for the first time a ROS dependent interaction between pAkt and IQGAP-1 in TNFalpha treated cells . Importantly , Akt inhibition not only reversed TNFalpha mediated changes in actin cytoskeletal organization but also abrogated anchorage independent growth . Together , these results suggest that TNFalpha induced oxidative stress affects Akt activation to regulate actin organization and growth of glioma cells .
    OUTPUT:
