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 Cisplatin chemotherapy often causes acute kidney injury in cancer patients . The causative mechanisms of cisplatin-induced acute kidney injury include renal inflammation , activation of p53 tumour suppressor protein and tubular apoptosis . Luteolin , a flavone found in medicinal herbs and plants , has been reported to exhibit anti-inflammatory , antioxidant and anticarcinogenic activities . The purpose of this study was to investigate the anti-apoptotic effect of luteolin on cisplatin-induced acute kidney injury and the molecular mechanism . METHODS C57BL/6 mice were treated with cisplatin ( 20 mg/kg ) with or without treatment with luteolin ( 50 mg/kg for 3 days ) . Renal function , histological changes , degree of oxidative stress and tubular apoptosis were examined . The effects of luteolin on cisplatin-induced expression of renal p53 , PUMA-Î± and Bcl-2 family proteins were evaluated . RESULTS Treatment of mice with cisplatin resulted in renal damage , showing an increase in blood urea nitrogen and creatinine levels , tubular damage , oxidative stress and apoptosis . Treatment of cisplatin-treated mice with luteolin significantly improved renal dysfunction , reducing tubular cell damage , oxidative stress and apoptosis . Examination of molecules involving apoptosis of the kidney revealed that treatment of cisplatin increased the levels of p53 and its phosphorylation , PUMA-Î± , Bax and caspase-3 activity that were significantly decreased by treatment with luteolin . CONCLUSION These results indicate that cisplatin induces acute kidney injury by regulation of p53-dependent renal tubular apoptosis and that luteolin ameliorates the cisplatin-mediated nephrotoxicity through down-regulation of p53-dependent apoptotic pathway in the kidney .
    OUTPUT:

agent
resisting cell death;tumor promoting inflammation
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 Cisplatin chemotherapy often causes acute kidney injury in cancer patients . The causative mechanisms of cisplatin-induced acute kidney injury include renal inflammation , activation of p53 tumour suppressor protein and tubular apoptosis . Luteolin , a flavone found in medicinal herbs and plants , has been reported to exhibit anti-inflammatory , antioxidant and anticarcinogenic activities . The purpose of this study was to investigate the anti-apoptotic effect of luteolin on cisplatin-induced acute kidney injury and the molecular mechanism . METHODS C57BL/6 mice were treated with cisplatin ( 20 mg/kg ) with or without treatment with luteolin ( 50 mg/kg for 3 days ) . Renal function , histological changes , degree of oxidative stress and tubular apoptosis were examined . The effects of luteolin on cisplatin-induced expression of renal p53 , PUMA-Î± and Bcl-2 family proteins were evaluated . RESULTS Treatment of mice with cisplatin resulted in renal damage , showing an increase in blood urea nitrogen and creatinine levels , tubular damage , oxidative stress and apoptosis . Treatment of cisplatin-treated mice with luteolin significantly improved renal dysfunction , reducing tubular cell damage , oxidative stress and apoptosis . Examination of molecules involving apoptosis of the kidney revealed that treatment of cisplatin increased the levels of p53 and its phosphorylation , PUMA-Î± , Bax and caspase-3 activity that were significantly decreased by treatment with luteolin . CONCLUSION These results indicate that cisplatin induces acute kidney injury by regulation of p53-dependent renal tubular apoptosis and that luteolin ameliorates the cisplatin-mediated nephrotoxicity through down-regulation of p53-dependent apoptotic pathway in the kidney .
    OUTPUT:
