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: Ultraviolet ( UV ) of sunlight is a complete carcinogen that can burn skin , enhance inflammation , and drive skin carcinogenesis . Previously , we have shown that sulforaphane ( SFN ) inhibited chemically induced skin carcinogenesis via nuclear factor ( erythroid-derived 2)-like 2 ( Nrf2 ) and others have shown that broccoli sprout extracts containing high SFN protected against UV-induced skin carcinogenesis in SKH-1 hairless mice . A recent study showed that there was no difference between Nrf2 knockout ( Nrf2 KO ) and Nrf2 wild-type ( WT ) BALB/C mice after exposing to high dose of UVB . Since Nrf2 plays critical roles in the anti-oxidative stress/anti-inflammatory responses , it is relevant to assess the role of Nrf2 for photoprotection against UV . In this context , the role of Nrf2 in UVB-induced skin inflammation in Nrf2 WT and Nrf2 KO C57BL/6 mice was studied . A single dose of UVB ( 300âmJ/cm(2) ) resulted in skin inflammation in both WT and Nrf2 KO ( -/- ) mice ( KO mice ) at 8âh and 8âd following UVB irradiation . In the WT mice inflammation returned to the basal level to a greater extent when compared to the KO mice . SFN treatment of Nrf2 WT but not Nrf2 KO mice restored the number of sunburn cells back to their basal level by 8âd after UVB irradiation . Additionally , UVB-induced short-term inflammatory biomarkers ( interleukin-1Î² and interleukin-6 ) were increased in the KO mice and UVB-induced apoptotic cells in the KO mice were significantly higher as compared to that in the WT . Taken together , our results show that functional Nrf2 confers a protective effect against UVB-induced inflammation , sunburn reaction , and SFN-mediated photoprotective effects in the skin .
    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: Ultraviolet ( UV ) of sunlight is a complete carcinogen that can burn skin , enhance inflammation , and drive skin carcinogenesis . Previously , we have shown that sulforaphane ( SFN ) inhibited chemically induced skin carcinogenesis via nuclear factor ( erythroid-derived 2)-like 2 ( Nrf2 ) and others have shown that broccoli sprout extracts containing high SFN protected against UV-induced skin carcinogenesis in SKH-1 hairless mice . A recent study showed that there was no difference between Nrf2 knockout ( Nrf2 KO ) and Nrf2 wild-type ( WT ) BALB/C mice after exposing to high dose of UVB . Since Nrf2 plays critical roles in the anti-oxidative stress/anti-inflammatory responses , it is relevant to assess the role of Nrf2 for photoprotection against UV . In this context , the role of Nrf2 in UVB-induced skin inflammation in Nrf2 WT and Nrf2 KO C57BL/6 mice was studied . A single dose of UVB ( 300âmJ/cm(2) ) resulted in skin inflammation in both WT and Nrf2 KO ( -/- ) mice ( KO mice ) at 8âh and 8âd following UVB irradiation . In the WT mice inflammation returned to the basal level to a greater extent when compared to the KO mice . SFN treatment of Nrf2 WT but not Nrf2 KO mice restored the number of sunburn cells back to their basal level by 8âd after UVB irradiation . Additionally , UVB-induced short-term inflammatory biomarkers ( interleukin-1Î² and interleukin-6 ) were increased in the KO mice and UVB-induced apoptotic cells in the KO mice were significantly higher as compared to that in the WT . Taken together , our results show that functional Nrf2 confers a protective effect against UVB-induced inflammation , sunburn reaction , and SFN-mediated photoprotective effects in the skin .
    OUTPUT:
