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: Quercetin is a flavonoid with anticancer properties . In this study , we examined the effects of quercetin on cell cycle , viability , and proliferation of cancer cells , either singly or in combination with the microtubule-targeting drugs taxol and nocodazole . Although quercetin induced cell death in a dose-dependent manner , 12.5-50 Î¼M quercetin inhibited the activity of both taxol and nocodazole to induce G2/M arrest in various cell lines . Quercetin also partially restored drug-induced loss in viability of treated cells for up to 72 h . This antagonism of microtubule-targeting drugs was accompanied by a delay in cell cycle progression and inhibition of the buildup of cyclin-B1 at the microtubule organizing center of treated cells . However , quercetin did not inhibit the microtubule targeting of taxol or nocodazole . Despite the short-term protection of cells by quercetin , colony formation and clonogenicity of HCT116 cells were still suppressed by quercetin or quercetin-taxol combination . The status of cell adherence to growth matrix was critical in determining the sensitivity of HCT116 cells to quercetin . We conclude that although long-term exposure of cancer cells to quercetin may prevent cell proliferation and survival , the interference of quercetin with cell cycle progression diminishes the efficacy of microtubule-targeting drugs to arrest cells at G2/M .
    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: Quercetin is a flavonoid with anticancer properties . In this study , we examined the effects of quercetin on cell cycle , viability , and proliferation of cancer cells , either singly or in combination with the microtubule-targeting drugs taxol and nocodazole . Although quercetin induced cell death in a dose-dependent manner , 12.5-50 Î¼M quercetin inhibited the activity of both taxol and nocodazole to induce G2/M arrest in various cell lines . Quercetin also partially restored drug-induced loss in viability of treated cells for up to 72 h . This antagonism of microtubule-targeting drugs was accompanied by a delay in cell cycle progression and inhibition of the buildup of cyclin-B1 at the microtubule organizing center of treated cells . However , quercetin did not inhibit the microtubule targeting of taxol or nocodazole . Despite the short-term protection of cells by quercetin , colony formation and clonogenicity of HCT116 cells were still suppressed by quercetin or quercetin-taxol combination . The status of cell adherence to growth matrix was critical in determining the sensitivity of HCT116 cells to quercetin . We conclude that although long-term exposure of cancer cells to quercetin may prevent cell proliferation and survival , the interference of quercetin with cell cycle progression diminishes the efficacy of microtubule-targeting drugs to arrest cells at G2/M .
    OUTPUT:
