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: Environmental or occupational exposure to low doses of arsenic induces a series of health problems including cancer . The molecular events in arsenic-induced carcinogenicity remain to be defined . In the NuLi-1 immortalized human lung epithelial cell line with p53 and pRb deficiency , exposure to low doses of arsenic trioxide for 72âh promoted cell proliferation and upregulated the gene transcription levels of FOXM1 , CDC6 , CDC25A , and cyclin D1 , which are both critical cell cycle regulatory genes and proto-oncogenes . Continuous in vitro exposure to 1âï¿½M arsenic trioxide for 34 wks induced malignant cell transformation , as evidenced by enhanced anchorage-independent cell growth . The expression of FOXM1 , CDC6 , CDC25A , and Cyclin D1 was dynamically elevated at the gene transcription and protein levels in the process of cell transformation . The carcinogenic ability of transformed cell colonies coincides with the expression levels of FOXM1 in in vitro anchorage-independent growth assays and in vivo tumor xenograft formation assays . In reverse , the knockdown of FOXM1 in lung adenocarcinoma A549 cells or arsenic-transformed NuLi-1 cells significantly decreased anchorage-independent cell growth and tumor xenograft formation . The transformed NuLi-1 cells showed genomic instability in the form of copy number variation ( CNV ) at chromosome 1 , 5 , 6 , 18 , and 20 , but not loss of heterozygosity ( LOH ) . These results showed for the first time that chronic exposure to low doses of arsenic trioxide promoted lung carcinogenicity , in part by aberrantly upregulating FOXM1 and its associated oncogenes , when the tumor suppressor genes p53 and pRb were inactivated. ï¿½ 2012 Wiley Periodicals , Inc .
    OUTPUT:

agent
evading growth suppressors;sustaining proliferative signaling
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: Environmental or occupational exposure to low doses of arsenic induces a series of health problems including cancer . The molecular events in arsenic-induced carcinogenicity remain to be defined . In the NuLi-1 immortalized human lung epithelial cell line with p53 and pRb deficiency , exposure to low doses of arsenic trioxide for 72âh promoted cell proliferation and upregulated the gene transcription levels of FOXM1 , CDC6 , CDC25A , and cyclin D1 , which are both critical cell cycle regulatory genes and proto-oncogenes . Continuous in vitro exposure to 1âï¿½M arsenic trioxide for 34 wks induced malignant cell transformation , as evidenced by enhanced anchorage-independent cell growth . The expression of FOXM1 , CDC6 , CDC25A , and Cyclin D1 was dynamically elevated at the gene transcription and protein levels in the process of cell transformation . The carcinogenic ability of transformed cell colonies coincides with the expression levels of FOXM1 in in vitro anchorage-independent growth assays and in vivo tumor xenograft formation assays . In reverse , the knockdown of FOXM1 in lung adenocarcinoma A549 cells or arsenic-transformed NuLi-1 cells significantly decreased anchorage-independent cell growth and tumor xenograft formation . The transformed NuLi-1 cells showed genomic instability in the form of copy number variation ( CNV ) at chromosome 1 , 5 , 6 , 18 , and 20 , but not loss of heterozygosity ( LOH ) . These results showed for the first time that chronic exposure to low doses of arsenic trioxide promoted lung carcinogenicity , in part by aberrantly upregulating FOXM1 and its associated oncogenes , when the tumor suppressor genes p53 and pRb were inactivated. ï¿½ 2012 Wiley Periodicals , Inc .
    OUTPUT:
