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: BACKGROUND Sorafenib has recently been shown to reduce tumour growth in hepatoblastoma ( HB ) xenografts . The effect of a combined administration with cytostatic agents was now investigated . METHODS Cell viability after treatment with sorafenib and different cytostatic agents was evaluated in two HB cell lines ( HUH6 and HepT1 ) using MTT assay . ERK signalling was investigated by western blot , NOXA expression by rt-PCR , and formation of DNA adducts using immunocytology . NMRI mice bearing subcutaneous HUH6-derived tumours were treated with sorafenib alone or in combination with cisplatin . Tumour progression , viability , apoptosis , and vascularisation were monitored by tumour volume , AFP levels , TUNEL assay , and CD31 immunostaining , respectively . RESULTS The combination of sorafenib and cisplatin led to a remarkable decrease in cell viability . The cisplatin-induced enhanced ERK1/2 activation , but not NOXA expression and the formation of DNA adducts was partly abrogated by sorafenib . In HB xenografts , both , sorafenib and alternated application of sorafenib and cisplatin significantly reduced tumour growth ( P&lt;0.05 ) . Levels of AFP were lower in both treated groups ( P=0.08 ) . Relative apoptotic areas were increased ( P=0.003 ) . Mean vascular density was the lowest in the sorafenib/CDDP group ( P=0.02 ) . CONCLUSION The combination of sorafenib with cisplatin might be a promising treatment option for high risk or recurrent HB .
    OUTPUT:

agent
genomic instability and mutation;resisting cell death
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: BACKGROUND Sorafenib has recently been shown to reduce tumour growth in hepatoblastoma ( HB ) xenografts . The effect of a combined administration with cytostatic agents was now investigated . METHODS Cell viability after treatment with sorafenib and different cytostatic agents was evaluated in two HB cell lines ( HUH6 and HepT1 ) using MTT assay . ERK signalling was investigated by western blot , NOXA expression by rt-PCR , and formation of DNA adducts using immunocytology . NMRI mice bearing subcutaneous HUH6-derived tumours were treated with sorafenib alone or in combination with cisplatin . Tumour progression , viability , apoptosis , and vascularisation were monitored by tumour volume , AFP levels , TUNEL assay , and CD31 immunostaining , respectively . RESULTS The combination of sorafenib and cisplatin led to a remarkable decrease in cell viability . The cisplatin-induced enhanced ERK1/2 activation , but not NOXA expression and the formation of DNA adducts was partly abrogated by sorafenib . In HB xenografts , both , sorafenib and alternated application of sorafenib and cisplatin significantly reduced tumour growth ( P&lt;0.05 ) . Levels of AFP were lower in both treated groups ( P=0.08 ) . Relative apoptotic areas were increased ( P=0.003 ) . Mean vascular density was the lowest in the sorafenib/CDDP group ( P=0.02 ) . CONCLUSION The combination of sorafenib with cisplatin might be a promising treatment option for high risk or recurrent HB .
    OUTPUT:
