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: Cigarette smoke ( CS ) is a rich source of radicals , predisposing the cell to oxidative stress resulting in inflammation . Chronic inflammation is a recognized risk factor for carcinogenesis . Cyclooxygenase-2 ( COX-2 ) is a mediator of inflammatory pathway and may , therefore , contribute to carcinogenesis . There are several reports that suggest the association between CS and COX-2 associated risk to cancer . In the present study , we examined the role of celecoxib ( a selective COX-2 inhibitor ) in modulating the oxidative stress caused by CS inhalation in mice . CS exposure for a period of 10 weeks caused oxidative stress in the pulmonary and hepatic tissues , as evident from the increase in lipid peroxidation levels ( LPO ) and decrease in reduced glutathione ( GSH ) levels . Celecoxib ( 125 mg/kg body weight for 8 weeks ) administration to CS inhaling mice reduced the oxidative stress by decreasing the LPO levels and enhancing the GSH levels in comparison to the CS-exposed group . CS exposure repressed the enzymatic antioxidant defense system , as evident from the decrease in catalase ( CAT ) and superoxide dismutase ( SOD ) activities . Co-adminstration of celecoxib considerably reversed the changes in the enzymatic antioxidant defense system . Histopathological studies of lungs showed that CS exposure induced alveolar wall destruction and air space enlargement . In co-treated group , the alveolar septa were thicker than normal with apparent infiltration of inflammatory cells . In CS-exposed group , hepatic tissue exhibited vacuolization and macrophage infiltration . Co-treatment with celecoxib restored the normal histoarchitechture in hepatic tissues of CS inhaling mice . Thus , the present study demonstrated that celecoxib adminstration reduced the oxidative stress-mediated risk to carcinogenesis , due to its ability to boost the antioxidant defense system .
    OUTPUT:

agent
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.
    ###
    INPUT: Cigarette smoke ( CS ) is a rich source of radicals , predisposing the cell to oxidative stress resulting in inflammation . Chronic inflammation is a recognized risk factor for carcinogenesis . Cyclooxygenase-2 ( COX-2 ) is a mediator of inflammatory pathway and may , therefore , contribute to carcinogenesis . There are several reports that suggest the association between CS and COX-2 associated risk to cancer . In the present study , we examined the role of celecoxib ( a selective COX-2 inhibitor ) in modulating the oxidative stress caused by CS inhalation in mice . CS exposure for a period of 10 weeks caused oxidative stress in the pulmonary and hepatic tissues , as evident from the increase in lipid peroxidation levels ( LPO ) and decrease in reduced glutathione ( GSH ) levels . Celecoxib ( 125 mg/kg body weight for 8 weeks ) administration to CS inhaling mice reduced the oxidative stress by decreasing the LPO levels and enhancing the GSH levels in comparison to the CS-exposed group . CS exposure repressed the enzymatic antioxidant defense system , as evident from the decrease in catalase ( CAT ) and superoxide dismutase ( SOD ) activities . Co-adminstration of celecoxib considerably reversed the changes in the enzymatic antioxidant defense system . Histopathological studies of lungs showed that CS exposure induced alveolar wall destruction and air space enlargement . In co-treated group , the alveolar septa were thicker than normal with apparent infiltration of inflammatory cells . In CS-exposed group , hepatic tissue exhibited vacuolization and macrophage infiltration . Co-treatment with celecoxib restored the normal histoarchitechture in hepatic tissues of CS inhaling mice . Thus , the present study demonstrated that celecoxib adminstration reduced the oxidative stress-mediated risk to carcinogenesis , due to its ability to boost the antioxidant defense system .
    OUTPUT:
