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 Epidemiologic data have shown that obesity independently increases colorectal cancer ( CRC ) risk , but the mechanisms are poorly understood . Obesity is an inflammatory state , and chronic colonic inflammation induces CRC . OBJECTIVE We conducted this proof-of-principle study to seek evidence of obesity-associated colorectal inflammation and to evaluate effects of diet-induced weight loss . DESIGN We measured inflammatory cytokines , gene arrays , and macrophage infiltration in rectosigmoid mucosal biopsies of 10 obese premenopausal women [ mean Â± SD body mass index ( in kg/m(2) ) : 35 Â± 3.5 ] before and after weight loss induced by a very-low-calorie diet . RESULTS Subjects lost a mean ( Â±SD ) of 10.1 Â± 1% of their initial weight . Weight loss significantly reduced fasting blood glucose , total cholesterol , triglycerides , LDL , tumor necrosis factor-Î± ( TNF-Î± ) , and interleukin ( IL)-8 concentrations ( P &lt ; 0.05 ) . After weight loss , rectosigmoid biopsies showed a 25-57% reduction in TNF-Î± , IL-1Î² , IL-8 , and monocyte chemotactic protein 1 concentrations ( P &lt ; 0.05 ) . T cell and macrophage counts decreased by 28% and 42% , respectively ( P &lt ; 0.05 ) . Gene arrays showed dramatic down-regulation of proinflammatory cytokine and chemokine pathways , prostaglandin metabolism , and the transcription factors STAT3 ( signal transducer and activator of transcription 3 ) and nuclear transcription factor ÎºB . Weight loss reduced expression of FOS and JUN genes and down-regulated oxidative stress pathways and the transcription factors ATF ( activating transcription factor ) and CREB ( cyclic AMP response element-binding ) . CONCLUSIONS Our data show that diet-induced weight loss in obese individuals reduces colorectal inflammation and greatly modulates inflammatory and cancer-related gene pathways . These data imply that obesity is accompanied by inflammation in the colorectal mucosa and that diet-induced weight loss reduces this inflammatory state and may thereby lower CRC risk .
    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.
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    INPUT: BACKGROUND Epidemiologic data have shown that obesity independently increases colorectal cancer ( CRC ) risk , but the mechanisms are poorly understood . Obesity is an inflammatory state , and chronic colonic inflammation induces CRC . OBJECTIVE We conducted this proof-of-principle study to seek evidence of obesity-associated colorectal inflammation and to evaluate effects of diet-induced weight loss . DESIGN We measured inflammatory cytokines , gene arrays , and macrophage infiltration in rectosigmoid mucosal biopsies of 10 obese premenopausal women [ mean Â± SD body mass index ( in kg/m(2) ) : 35 Â± 3.5 ] before and after weight loss induced by a very-low-calorie diet . RESULTS Subjects lost a mean ( Â±SD ) of 10.1 Â± 1% of their initial weight . Weight loss significantly reduced fasting blood glucose , total cholesterol , triglycerides , LDL , tumor necrosis factor-Î± ( TNF-Î± ) , and interleukin ( IL)-8 concentrations ( P &lt ; 0.05 ) . After weight loss , rectosigmoid biopsies showed a 25-57% reduction in TNF-Î± , IL-1Î² , IL-8 , and monocyte chemotactic protein 1 concentrations ( P &lt ; 0.05 ) . T cell and macrophage counts decreased by 28% and 42% , respectively ( P &lt ; 0.05 ) . Gene arrays showed dramatic down-regulation of proinflammatory cytokine and chemokine pathways , prostaglandin metabolism , and the transcription factors STAT3 ( signal transducer and activator of transcription 3 ) and nuclear transcription factor ÎºB . Weight loss reduced expression of FOS and JUN genes and down-regulated oxidative stress pathways and the transcription factors ATF ( activating transcription factor ) and CREB ( cyclic AMP response element-binding ) . CONCLUSIONS Our data show that diet-induced weight loss in obese individuals reduces colorectal inflammation and greatly modulates inflammatory and cancer-related gene pathways . These data imply that obesity is accompanied by inflammation in the colorectal mucosa and that diet-induced weight loss reduces this inflammatory state and may thereby lower CRC risk .
    OUTPUT:
