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: The present study was designed to investigate the protective efficacy of eugenol against skin cancer and probe into the mechanistic aspects . Skin tumors were initiated by applying 160 nmol DMBA and promoted by twice weekly applications of 8.5 nmol TPA for 28 wk . All mice developed tumors by 13 wk of promotion . However , in mice pretreated with 30 microL eugenol , no tumors were detected until 8 wk ( following anti-initiation protocol ) and until 14 wk ( following antipromotion protocol ) of tumor promotion . PCNA and TUNEL immunohistochemistry of tumors revealed eugenol to ameliorate cell proliferation and elevate apoptosis respectively . The effect of eugenol was assessed on specific stages of carcinogenesis . Initiation with DMBA led to a significant upregulation of p53 expression with a concomitant increase in p21(WAF1) levels in epidermal cells indicating induction of damage to the DNA . However , pretreatment with eugenol led to overexpression of these genes , which probably helped stimulate apoptosis of the initiated cells . To ascertain the molecular mechanisms implicated in the antitumor promoting activity of eugenol , its effect was investigated on markers of tumor promotion and inflammation : ODC activity and iNOS and COX-2 expression , and on levels of proinflammatory cytokines ( IL-6 , TNF-alpha , and PGE(2) ) . Eugenol markedly inhibited all . Eugenol also inhibited the upstream signaling molecule : NF-kappaB , which regulates the expression of these genes . TPA-induced depletion of cutaneous GSH and antioxidant enzymes armory was also precluded by eugenol . From these results , it could be concluded that eugenol markedly protects against chemically induced skin cancer and acts possibly by virtue of its antiproliferative , anti-inflammatory , and antioxidant activities .
    OUTPUT:

agent
resisting cell death;sustaining proliferative signaling;evading growth suppressors;genomic instability and mutation;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: The present study was designed to investigate the protective efficacy of eugenol against skin cancer and probe into the mechanistic aspects . Skin tumors were initiated by applying 160 nmol DMBA and promoted by twice weekly applications of 8.5 nmol TPA for 28 wk . All mice developed tumors by 13 wk of promotion . However , in mice pretreated with 30 microL eugenol , no tumors were detected until 8 wk ( following anti-initiation protocol ) and until 14 wk ( following antipromotion protocol ) of tumor promotion . PCNA and TUNEL immunohistochemistry of tumors revealed eugenol to ameliorate cell proliferation and elevate apoptosis respectively . The effect of eugenol was assessed on specific stages of carcinogenesis . Initiation with DMBA led to a significant upregulation of p53 expression with a concomitant increase in p21(WAF1) levels in epidermal cells indicating induction of damage to the DNA . However , pretreatment with eugenol led to overexpression of these genes , which probably helped stimulate apoptosis of the initiated cells . To ascertain the molecular mechanisms implicated in the antitumor promoting activity of eugenol , its effect was investigated on markers of tumor promotion and inflammation : ODC activity and iNOS and COX-2 expression , and on levels of proinflammatory cytokines ( IL-6 , TNF-alpha , and PGE(2) ) . Eugenol markedly inhibited all . Eugenol also inhibited the upstream signaling molecule : NF-kappaB , which regulates the expression of these genes . TPA-induced depletion of cutaneous GSH and antioxidant enzymes armory was also precluded by eugenol . From these results , it could be concluded that eugenol markedly protects against chemically induced skin cancer and acts possibly by virtue of its antiproliferative , anti-inflammatory , and antioxidant activities .
    OUTPUT:
