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: We recently isolated an exon-4-deleted epidermal growth factor receptor ( EGFR ) variant , termed de4 EGFR . Because the extracellular domain alteration of receptors often influences the antitumor effect of therapeutic antibodies , it is essential to test the sensitivity of de4 EGFR(+) tumors to anti-EGFR antibodies . Therefore , in this study , the antitumor activities of mAb CH12 , an anti-EGFRvIII antibody developed in our laboratory , as well as a U.S. Food and Drug Administration-approved anti-EGFR antibody , cetuximab ( C225 ) , were characterized on de4 EGFR(+) models . The results of FACS assays showed that CH12 bound to de4 EGFR with a higher avidity than did C225 . Interestingly , CH12 , but not C225 , significantly inhibited the metastasis and growth of U87MG-de4 EGFR xenografts , with a growth-inhibition ratio of 46.48% in vivo , and prolonged the survival of the tumor-bearing mice by 37.2% . Treatment with CH12 significantly suppressed tumor proliferation and angiogenesis with increased tumor apoptosis . Mechanistically , de4 EGFR protein expression was virtually undetectable in the U87MG-de4 EGFR xenografts treated with CH12 . This may account for the observed reduction of Akt and Erk phosphorylation , cyclin D1 , Bcl-2 , and Bcl-x(L) expression and the increase of p27 and E-cadherin expression . Intriguingly , LAMP-1 , a major component of the lysosome , was significantly up-regulated in the CH12-treated group but not in the C225-treated group , suggesting its contribution to the degradation of de4 EGFR . Taken together , our data demonstrated that mAb CH12 is a promising therapeutic agent for treating de4 EGFR(+) gliomas .
    OUTPUT:

agent
activating invasion and metastasis;inducing angiogenesis;resisting cell death;sustaining proliferative signaling
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: We recently isolated an exon-4-deleted epidermal growth factor receptor ( EGFR ) variant , termed de4 EGFR . Because the extracellular domain alteration of receptors often influences the antitumor effect of therapeutic antibodies , it is essential to test the sensitivity of de4 EGFR(+) tumors to anti-EGFR antibodies . Therefore , in this study , the antitumor activities of mAb CH12 , an anti-EGFRvIII antibody developed in our laboratory , as well as a U.S. Food and Drug Administration-approved anti-EGFR antibody , cetuximab ( C225 ) , were characterized on de4 EGFR(+) models . The results of FACS assays showed that CH12 bound to de4 EGFR with a higher avidity than did C225 . Interestingly , CH12 , but not C225 , significantly inhibited the metastasis and growth of U87MG-de4 EGFR xenografts , with a growth-inhibition ratio of 46.48% in vivo , and prolonged the survival of the tumor-bearing mice by 37.2% . Treatment with CH12 significantly suppressed tumor proliferation and angiogenesis with increased tumor apoptosis . Mechanistically , de4 EGFR protein expression was virtually undetectable in the U87MG-de4 EGFR xenografts treated with CH12 . This may account for the observed reduction of Akt and Erk phosphorylation , cyclin D1 , Bcl-2 , and Bcl-x(L) expression and the increase of p27 and E-cadherin expression . Intriguingly , LAMP-1 , a major component of the lysosome , was significantly up-regulated in the CH12-treated group but not in the C225-treated group , suggesting its contribution to the degradation of de4 EGFR . Taken together , our data demonstrated that mAb CH12 is a promising therapeutic agent for treating de4 EGFR(+) gliomas .
    OUTPUT:
