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: An acquired mutation ( T790M ) in the epidermal growth factor receptor ( EGFR ) accounts for half of all relapses in non-small cell lung cancer ( NSCLC ) patients who initially respond to EGFR kinase inhibitors . In this study , we demonstrated for the first time that EGFR-T790M interacts with the cytoskeletal components , myosin heavy chain 9 ( MYH9 ) and Î²-actin , in the nucleus of H1975 cells carrying the T790M-mutant EGFR . The interactions of EGFR with MYH9 and Î²-actin were reduced in the presence of blebbistatin , a specific inhibitor for the MYH9-Î²-actin interaction , suggesting that the EGFR interaction with MYH9 and Î²-actin is affected by the integrity of the cytoskeleton . These physical interactions among MYH9 , Î²-actin , and EGFR were also impaired by CL-387,785 , a kinase inhibitor for EGFR-T790M . Furthermore , CL-387,785 and blebbistatin interacted in a synergistic fashion to suppress cell proliferation and induce apoptosis in H1975 cells . The combination of CL-387,785 and blebbistatin enhanced the down-regulation of cyclooxygenase-2 ( COX-2 ) , a transcriptional target of nuclear EGFR . Overall , our findings demonstrate that disrupting EGFR interactions with the cytoskeletal components enhanced the anti-cancer effects of CL-387,785 against H1975 cells , suggesting a novel therapeutic approach for NSCLC cells that express the drug-resistant EGFR-T790M .
    OUTPUT:

agent
sustaining proliferative signaling;resisting cell death
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: An acquired mutation ( T790M ) in the epidermal growth factor receptor ( EGFR ) accounts for half of all relapses in non-small cell lung cancer ( NSCLC ) patients who initially respond to EGFR kinase inhibitors . In this study , we demonstrated for the first time that EGFR-T790M interacts with the cytoskeletal components , myosin heavy chain 9 ( MYH9 ) and Î²-actin , in the nucleus of H1975 cells carrying the T790M-mutant EGFR . The interactions of EGFR with MYH9 and Î²-actin were reduced in the presence of blebbistatin , a specific inhibitor for the MYH9-Î²-actin interaction , suggesting that the EGFR interaction with MYH9 and Î²-actin is affected by the integrity of the cytoskeleton . These physical interactions among MYH9 , Î²-actin , and EGFR were also impaired by CL-387,785 , a kinase inhibitor for EGFR-T790M . Furthermore , CL-387,785 and blebbistatin interacted in a synergistic fashion to suppress cell proliferation and induce apoptosis in H1975 cells . The combination of CL-387,785 and blebbistatin enhanced the down-regulation of cyclooxygenase-2 ( COX-2 ) , a transcriptional target of nuclear EGFR . Overall , our findings demonstrate that disrupting EGFR interactions with the cytoskeletal components enhanced the anti-cancer effects of CL-387,785 against H1975 cells , suggesting a novel therapeutic approach for NSCLC cells that express the drug-resistant EGFR-T790M .
    OUTPUT:
