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: OBJECTIVE Overexpression of epidermal growth factor receptor ( EGFR ) in glioblastoma multiforme ( GBM ) secondary to EGFR gene amplification is associated with a more aggressive tumor phenotype and a worse clinical outcome . The purpose of this study was to analyze whether blocking this receptor with the anti-EGFR chimeric monoclonal antibody C225 would decrease proliferation and increase apoptosis in GBM cells . METHODS EGFR expression and amplification were analyzed for seven human GBM cell lines . These lines were then exposed to different concentrations of C225 for 48 hours , 72 hours , and 7 days , after which time cytotoxicity , apoptosis , and vascular endothelial growth factor expression were assessed in vitro . Two EGFR-amplified human GBM were implanted in the flanks of nude mice , and the animals received C225 twice per week intraperitoneally for 5 weeks . Tumor volumes and survival times were compared with those of sham-treated mice . RESULTS EGFR gene amplification was demonstrated in three of the primary GBM lines . C225 treatment produced significant cytotoxicity in all three EGFR-amplified GBM lines , but not in unamplified lines . Flow cytometry demonstrated increased apoptosis in C225-treated , EGFR-amplified GBM lines , but not in unamplified lines . There was a decrease in vascular endothelial growth factor expression in all GBM lines with exposure to C225 . Tumor-bearing mice treated with C225 experienced significant inhibition of tumor growth as well as a 200% increase in median survival . CONCLUSION Blocking EGFR in GBM cells that overexpress this receptor significantly changes tumor cell biology by promoting apoptosis while decreasing proliferation and vascular endothelial growth factor expression . This approach holds great promise for the treatment of patients with GBMs .
    OUTPUT:

agent
sustaining proliferative signaling;resisting cell death;inducing angiogenesis
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: OBJECTIVE Overexpression of epidermal growth factor receptor ( EGFR ) in glioblastoma multiforme ( GBM ) secondary to EGFR gene amplification is associated with a more aggressive tumor phenotype and a worse clinical outcome . The purpose of this study was to analyze whether blocking this receptor with the anti-EGFR chimeric monoclonal antibody C225 would decrease proliferation and increase apoptosis in GBM cells . METHODS EGFR expression and amplification were analyzed for seven human GBM cell lines . These lines were then exposed to different concentrations of C225 for 48 hours , 72 hours , and 7 days , after which time cytotoxicity , apoptosis , and vascular endothelial growth factor expression were assessed in vitro . Two EGFR-amplified human GBM were implanted in the flanks of nude mice , and the animals received C225 twice per week intraperitoneally for 5 weeks . Tumor volumes and survival times were compared with those of sham-treated mice . RESULTS EGFR gene amplification was demonstrated in three of the primary GBM lines . C225 treatment produced significant cytotoxicity in all three EGFR-amplified GBM lines , but not in unamplified lines . Flow cytometry demonstrated increased apoptosis in C225-treated , EGFR-amplified GBM lines , but not in unamplified lines . There was a decrease in vascular endothelial growth factor expression in all GBM lines with exposure to C225 . Tumor-bearing mice treated with C225 experienced significant inhibition of tumor growth as well as a 200% increase in median survival . CONCLUSION Blocking EGFR in GBM cells that overexpress this receptor significantly changes tumor cell biology by promoting apoptosis while decreasing proliferation and vascular endothelial growth factor expression . This approach holds great promise for the treatment of patients with GBMs .
    OUTPUT:
