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: Amplification of the HER-2 ( c-erbB-2 ) gene and overexpression of the p185HER-2 gene product is found in approximately one-third of primary human breast and ovarian cancers and is associated with a poor clinical outcome of early relapse and death . The HER-2 gene encodes a cell-surface growth factor receptor with intrinsic tyrosine kinase activity . Wild-type human HER-2 has been shown to act as a potent oncogene when over-expressed in mouse fibroblasts . Recent data suggest that the mechanism by which HER-2 mediates transformation requires the interaction of the epidermal growth factor ( EGF ) receptor . To test whether overexpression of normal human HER-2 can transform cells independently of the EGF receptor , we have introduced multiple copies of HER-2 into the EGF receptor-negative cell line , NR6 , and have performed assays for both transformation and tumorigenicity . Engineered NR6 cells that overexpress the HER-2 gene product display a highly transformed and tumorigenic phenotype as compared with control cells . Additionally , a monoclonal antibody to the extracellular domain of the HER-2 receptor is able to inhibit the proliferation of the overexpressing cells in vitro as well as tumor growth in vivo . This study provides clear evidence that HER-2-mediated transformation can be achieved independently of the EGF receptor .
    OUTPUT:

agent
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.
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    INPUT: Amplification of the HER-2 ( c-erbB-2 ) gene and overexpression of the p185HER-2 gene product is found in approximately one-third of primary human breast and ovarian cancers and is associated with a poor clinical outcome of early relapse and death . The HER-2 gene encodes a cell-surface growth factor receptor with intrinsic tyrosine kinase activity . Wild-type human HER-2 has been shown to act as a potent oncogene when over-expressed in mouse fibroblasts . Recent data suggest that the mechanism by which HER-2 mediates transformation requires the interaction of the epidermal growth factor ( EGF ) receptor . To test whether overexpression of normal human HER-2 can transform cells independently of the EGF receptor , we have introduced multiple copies of HER-2 into the EGF receptor-negative cell line , NR6 , and have performed assays for both transformation and tumorigenicity . Engineered NR6 cells that overexpress the HER-2 gene product display a highly transformed and tumorigenic phenotype as compared with control cells . Additionally , a monoclonal antibody to the extracellular domain of the HER-2 receptor is able to inhibit the proliferation of the overexpressing cells in vitro as well as tumor growth in vivo . This study provides clear evidence that HER-2-mediated transformation can be achieved independently of the EGF receptor .
    OUTPUT:
