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: Inorganic arsenic in the drinking water is a multisite human carcinogen that potentially targets the kidney . Recent evidence also indicates that developmental arsenic exposure impacts renal carcinogenesis in humans and mice . Emerging theory indicates that cancer may be a disease of stem cells ( SCs ) and that there are abundant active SCs during early life . Therefore , we hypothesized that inorganic arsenic targets SCs , or partially differentiated progenitor cells ( PCs ) , for oncogenic transformation . Thus , a rat kidney SC/PC cell line , RIMM-18 , was chronically exposed to low-level arsenite ( 500 nM ) for up to 28 weeks . Multiple markers of acquired cancer phenotype were assessed biweekly during arsenic exposure , including secreted matrix metalloproteinase ( MMP ) activity , proliferation rate , colony formation in soft agar , and cellular invasiveness . Arsenic exposure by 10 weeks and after also induced marked and sustained increases in colony formation , indicative of the loss of contact inhibition , and increased invasiveness , both cancer cell characteristics . Compared to the passage-matched control , chronic arsenic exposure caused exposure-duration dependent increases in secreted MMP-2 and MMP-9 activity , Cox-2 expression , and more rapid proliferation ( all &gt;2-fold ) , characteristics typical of cancer cells . Dysregulation of SC maintenance genes and signaling pathways are common during oncogenesis . During arsenite exposure , expression of several genes associated with normal kidney development and SC regulation and differentiation ( i.e. , Wt-1 , Wnt-4 , Bmp-7 , etc. ) were aberrantly altered . Arsenic-exposed renal SCs produced more nonadherent spheroid bodies that grew much more aggressively in Matrigel , typical of cancer SCs ( CSCs ) . The transformed cells also showed gene overexpression typical of renal SCs/CSCs ( CD24 , Osr1 , Ncam ) and arsenic adaptation such as overexpression of Mt-1 , Mt2 , Sod-1 , and Abcc2 . These data suggest that inorganic arsenic induced an acquired cancer phenotype in vitro in these rat kidney SCs potentially forming CSCs and , consistent with data in vivo , indicate that these multipotent SCs may be targets of arsenic during renal carcinogenesis .
    OUTPUT:

agent
activating invasion and metastasis;evading growth suppressors;sustaining proliferative signaling;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: Inorganic arsenic in the drinking water is a multisite human carcinogen that potentially targets the kidney . Recent evidence also indicates that developmental arsenic exposure impacts renal carcinogenesis in humans and mice . Emerging theory indicates that cancer may be a disease of stem cells ( SCs ) and that there are abundant active SCs during early life . Therefore , we hypothesized that inorganic arsenic targets SCs , or partially differentiated progenitor cells ( PCs ) , for oncogenic transformation . Thus , a rat kidney SC/PC cell line , RIMM-18 , was chronically exposed to low-level arsenite ( 500 nM ) for up to 28 weeks . Multiple markers of acquired cancer phenotype were assessed biweekly during arsenic exposure , including secreted matrix metalloproteinase ( MMP ) activity , proliferation rate , colony formation in soft agar , and cellular invasiveness . Arsenic exposure by 10 weeks and after also induced marked and sustained increases in colony formation , indicative of the loss of contact inhibition , and increased invasiveness , both cancer cell characteristics . Compared to the passage-matched control , chronic arsenic exposure caused exposure-duration dependent increases in secreted MMP-2 and MMP-9 activity , Cox-2 expression , and more rapid proliferation ( all &gt;2-fold ) , characteristics typical of cancer cells . Dysregulation of SC maintenance genes and signaling pathways are common during oncogenesis . During arsenite exposure , expression of several genes associated with normal kidney development and SC regulation and differentiation ( i.e. , Wt-1 , Wnt-4 , Bmp-7 , etc. ) were aberrantly altered . Arsenic-exposed renal SCs produced more nonadherent spheroid bodies that grew much more aggressively in Matrigel , typical of cancer SCs ( CSCs ) . The transformed cells also showed gene overexpression typical of renal SCs/CSCs ( CD24 , Osr1 , Ncam ) and arsenic adaptation such as overexpression of Mt-1 , Mt2 , Sod-1 , and Abcc2 . These data suggest that inorganic arsenic induced an acquired cancer phenotype in vitro in these rat kidney SCs potentially forming CSCs and , consistent with data in vivo , indicate that these multipotent SCs may be targets of arsenic during renal carcinogenesis .
    OUTPUT:
