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: PTEN , a phosphoinositide-3-phosphatase , serves dual roles as a tumor suppressor and regulator of cellular anabolic/catabolic metabolism . Adaptation of a redox-sensitive cysteinyl thiol in PTEN for signal transduction by hydrogen peroxide may have superimposed a vulnerability to other mediators of oxidative stress and inflammation , especially reactive carbonyl species , which are commonly occurring by-products of arachidonic acid peroxidation . Using MCF7 and HEK-293 cells , we report that several reactive aldehydes and ketones , e.g. electrophilic Î±,Î²-enals ( acrolein , 4-hydroxy-2-nonenal ) and Î±,Î²-enones ( prostaglandin A(2) , Î12-prostaglandin J(2) and 15-deoxy-Î-12,14-prostaglandin J(2) ) covalently modify and inactivate cellular PTEN , with ensuing activation of PKB/Akt kinase ; phosphorylation of Akt substrates ; increased cell proliferation ; and increased nuclear Î²-catenin signaling . Alkylation of PTEN by Î±,Î²-enals/enones and interference with its restraint of cellular PKB/Akt signaling may accentuate hyperplastic and neoplastic disorders associated with chronic inflammation , oxidative stress , or aging .
    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: PTEN , a phosphoinositide-3-phosphatase , serves dual roles as a tumor suppressor and regulator of cellular anabolic/catabolic metabolism . Adaptation of a redox-sensitive cysteinyl thiol in PTEN for signal transduction by hydrogen peroxide may have superimposed a vulnerability to other mediators of oxidative stress and inflammation , especially reactive carbonyl species , which are commonly occurring by-products of arachidonic acid peroxidation . Using MCF7 and HEK-293 cells , we report that several reactive aldehydes and ketones , e.g. electrophilic Î±,Î²-enals ( acrolein , 4-hydroxy-2-nonenal ) and Î±,Î²-enones ( prostaglandin A(2) , Î12-prostaglandin J(2) and 15-deoxy-Î-12,14-prostaglandin J(2) ) covalently modify and inactivate cellular PTEN , with ensuing activation of PKB/Akt kinase ; phosphorylation of Akt substrates ; increased cell proliferation ; and increased nuclear Î²-catenin signaling . Alkylation of PTEN by Î±,Î²-enals/enones and interference with its restraint of cellular PKB/Akt signaling may accentuate hyperplastic and neoplastic disorders associated with chronic inflammation , oxidative stress , or aging .
    OUTPUT:
