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: The vascular endothelial growth factor ( VEGF ) receptor tyrosine kinase inhibitor sunitinib has been approved for first-line treatment of patients with metastatic renal cancer and is currently being trialled in other cancers . However , the effectiveness of this anti-angiogenic agent is limited by the presence of innate and acquired drug resistance . By screening a panel of candidate growth factors we identified fibroblast growth factor 2 ( FGF2 ) as a potent regulator of endothelial cell sensitivity to sunitinib . We show that FGF2 supports endothelial proliferation and de novo tubule formation in the presence of sunitinib and that FGF2 can suppress sunitinib-induced retraction of tubules . Importantly , these effects of FGF2 were ablated by PD173074 , a small molecule inhibitor of FGF receptor signalling . We also show that FGF2 can stimulate pro-angiogenic signalling pathways in endothelial cells despite the presence of sunitinib . Finally , analysis of clinical renal-cancer samples demonstrates that a large proportion of renal cancers strongly express FGF2 . We suggest that therapeutic strategies designed to simultaneously target both VEGF and FGF2 signalling may prove more efficacious than sunitinib in renal cancer patients whose tumours express FGF2 .
    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: The vascular endothelial growth factor ( VEGF ) receptor tyrosine kinase inhibitor sunitinib has been approved for first-line treatment of patients with metastatic renal cancer and is currently being trialled in other cancers . However , the effectiveness of this anti-angiogenic agent is limited by the presence of innate and acquired drug resistance . By screening a panel of candidate growth factors we identified fibroblast growth factor 2 ( FGF2 ) as a potent regulator of endothelial cell sensitivity to sunitinib . We show that FGF2 supports endothelial proliferation and de novo tubule formation in the presence of sunitinib and that FGF2 can suppress sunitinib-induced retraction of tubules . Importantly , these effects of FGF2 were ablated by PD173074 , a small molecule inhibitor of FGF receptor signalling . We also show that FGF2 can stimulate pro-angiogenic signalling pathways in endothelial cells despite the presence of sunitinib . Finally , analysis of clinical renal-cancer samples demonstrates that a large proportion of renal cancers strongly express FGF2 . We suggest that therapeutic strategies designed to simultaneously target both VEGF and FGF2 signalling may prove more efficacious than sunitinib in renal cancer patients whose tumours express FGF2 .
    OUTPUT:
