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: Accumulating data suggest arsenic may be an endocrine disruptor and tentatively linked to breast cancer by some studies . Therefore , we tested the effects of chronic inorganic arsenic exposure on the normal estrogen receptor ( ER)-negative breast epithelial cell line , MCF-10A . Cells were chronically exposed to a low-level arsenite ( 500nM ) for up to 24weeks . Markers of cancer cell phenotype and the expression of critical genes relevant to breast cancer or stem cells ( SCs ) were examined . After 24weeks , chronic arsenic-exposed breast epithelial ( CABE ) cells showed increases in secreted MMP activity , colony formation , invasion , and proliferation rate , indicating an acquired cancer cell phenotype . These CABE cells presented with basal-like breast cancer characteristics , including ER-Î± , HER-2 , and progesterone receptor negativity , and overexpression of K5 and p63 . Putative CD44(+)/CD24(-/low) breast SCs were increased to 80% over control in CABE cells . CABE cells also formed multilayer cell mounds , indicative of loss of contact inhibition . These mounds showed high levels of K5 and p63 , indicating the potential presence of cancer stem cells ( CSCs ) . Epithelial-to-mesenchymal transition occurred during arsenic exposure . Overexpression of aromatase , a key rate-limiting enzyme in estrogen synthesis , occurred with arsenic starting early on in exposure . Levels of 17Î²-estradiol increased in CABE cells and their conditioned medium . The aromatase inhibitor letrozole abolished arsenic-induced increases in 17Î²-estradiol production and reversed cancer cell phenotype . Thus , chronic arsenic exposure drives human breast epithelia into a cancer cell phenotype with an apparent overabundance of putative CSCs . Arsenic appears to transform breast epithelia through overexpression of aromatase , thereby activating oncogenic processes independent of ER .
    OUTPUT:

agent
activating invasion and metastasis;sustaining proliferative signaling;evading growth suppressors
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: Accumulating data suggest arsenic may be an endocrine disruptor and tentatively linked to breast cancer by some studies . Therefore , we tested the effects of chronic inorganic arsenic exposure on the normal estrogen receptor ( ER)-negative breast epithelial cell line , MCF-10A . Cells were chronically exposed to a low-level arsenite ( 500nM ) for up to 24weeks . Markers of cancer cell phenotype and the expression of critical genes relevant to breast cancer or stem cells ( SCs ) were examined . After 24weeks , chronic arsenic-exposed breast epithelial ( CABE ) cells showed increases in secreted MMP activity , colony formation , invasion , and proliferation rate , indicating an acquired cancer cell phenotype . These CABE cells presented with basal-like breast cancer characteristics , including ER-Î± , HER-2 , and progesterone receptor negativity , and overexpression of K5 and p63 . Putative CD44(+)/CD24(-/low) breast SCs were increased to 80% over control in CABE cells . CABE cells also formed multilayer cell mounds , indicative of loss of contact inhibition . These mounds showed high levels of K5 and p63 , indicating the potential presence of cancer stem cells ( CSCs ) . Epithelial-to-mesenchymal transition occurred during arsenic exposure . Overexpression of aromatase , a key rate-limiting enzyme in estrogen synthesis , occurred with arsenic starting early on in exposure . Levels of 17Î²-estradiol increased in CABE cells and their conditioned medium . The aromatase inhibitor letrozole abolished arsenic-induced increases in 17Î²-estradiol production and reversed cancer cell phenotype . Thus , chronic arsenic exposure drives human breast epithelia into a cancer cell phenotype with an apparent overabundance of putative CSCs . Arsenic appears to transform breast epithelia through overexpression of aromatase , thereby activating oncogenic processes independent of ER .
    OUTPUT:
