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: Progression of breast cancer is associated with remodeling of the extracellular matrix , often involving a switch from estrogen dependence to a dependence on EGF receptor ( EGFR)/HER-2 and is accompanied by increased expression of the main binding protein for insulin-like growth factors ( IGFBP-3 ) . We have examined the effects of IGFBP-3 on EGF responses of breast epithelial cells in the context of changes in the extracellular matrix . On plastic and laminin with MCF-10A normal breast epithelial cells , EGF and IGFBP-3 each increased cell growth and together produced a synergistic response , whereas with T47D breast cancer cells IGFBP-3 alone had no effect , but the ability of EGF to increase cell proliferation was markedly inhibited in the presence of IGFBP-3 . In contrast on fibronectin with MCF-10A cells , IGFBP-3 alone inhibited cell growth and blocked EGF-induced proliferation . With the cancer cells , IGFBP-3 alone had no effect but enhanced the EGF-induced increase in cell growth . The insulin-like growth factor-independent effects of IGFBP-3 alone on cell proliferation were completely abrogated in the presence of an EGFR , tyrosine kinase inhibitor , Iressa . Although IGFBP-3 did not affect EGFR phosphorylation [ Tyr(1068) ] , it was found to modulate receptor internalization and was associated with activation of Rho and subsequent changes in MAPK phosphorylation . The levels of fibronectin and IGFBP-3 within breast tumors may determine their dependence on EGFR and their response to therapies targeting this 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.
    ###
    INPUT: Progression of breast cancer is associated with remodeling of the extracellular matrix , often involving a switch from estrogen dependence to a dependence on EGF receptor ( EGFR)/HER-2 and is accompanied by increased expression of the main binding protein for insulin-like growth factors ( IGFBP-3 ) . We have examined the effects of IGFBP-3 on EGF responses of breast epithelial cells in the context of changes in the extracellular matrix . On plastic and laminin with MCF-10A normal breast epithelial cells , EGF and IGFBP-3 each increased cell growth and together produced a synergistic response , whereas with T47D breast cancer cells IGFBP-3 alone had no effect , but the ability of EGF to increase cell proliferation was markedly inhibited in the presence of IGFBP-3 . In contrast on fibronectin with MCF-10A cells , IGFBP-3 alone inhibited cell growth and blocked EGF-induced proliferation . With the cancer cells , IGFBP-3 alone had no effect but enhanced the EGF-induced increase in cell growth . The insulin-like growth factor-independent effects of IGFBP-3 alone on cell proliferation were completely abrogated in the presence of an EGFR , tyrosine kinase inhibitor , Iressa . Although IGFBP-3 did not affect EGFR phosphorylation [ Tyr(1068) ] , it was found to modulate receptor internalization and was associated with activation of Rho and subsequent changes in MAPK phosphorylation . The levels of fibronectin and IGFBP-3 within breast tumors may determine their dependence on EGFR and their response to therapies targeting this receptor .
    OUTPUT:
