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: Elevated phosphorylation of estrogen receptor Î± ( ERÎ± ) at serines 118 ( S118 ) and 167 ( S167 ) is associated with favorable outcome for tamoxifen adjuvant therapy and may serve as surrogate markers for a functional ERÎ± signaling pathway in breast cancer . It is possible that loss of phosphorylation at S118 and/or S167 could disrupt ERÎ± signaling , resulting in aggressive ERÎ±-independent breast cancer cells . To this end , MCF-7 breast cancer cells were stably transfected with an ERÎ±-specific short hairpin RNA that reduced endogenous ERÎ± . The resulting cell line was stably transfected with wild-type ERÎ± ( ER-AB cells ) , or ERÎ± containing serine to alanine mutation at S118 or S167 ( S118A cells and S167A cells , respectively ) . These stable cell lines expressed approximately equivalent ERÎ± compared with parental MCF-7 cells and were evaluated for growth , morphology , migration/invasion , and ERÎ±-regulated gene expression . S118A cells and S167A cells exhibited increased growth and migration/invasion in vitro . Forward- and side-scatter flow cytometry revealed that S167A cells were smaller in size , and both S118A and S167A cells exhibited less cellular complexity . S118A and S167A cells expressed pancytokeratin and membrane localization of Î²-catenin and did not express vimentin , indicating retention of epithelial lineage markers . Expression of ERÎ±-target genes and other genes regulated by ERÎ± signaling or involved in breast cancer were markedly altered in both S118A and S167A cells . In summary , attenuated phosphorylation of ERÎ± at S118 and S167 significantly affected cellular physiology and behavior in MCF-7 breast cancer cells , resulting in increased growth , migration/invasion , compromised expression of ERÎ± target genes , and markedly altered gene expression patterns .
    OUTPUT:

agent
activating invasion and metastasis
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: Elevated phosphorylation of estrogen receptor Î± ( ERÎ± ) at serines 118 ( S118 ) and 167 ( S167 ) is associated with favorable outcome for tamoxifen adjuvant therapy and may serve as surrogate markers for a functional ERÎ± signaling pathway in breast cancer . It is possible that loss of phosphorylation at S118 and/or S167 could disrupt ERÎ± signaling , resulting in aggressive ERÎ±-independent breast cancer cells . To this end , MCF-7 breast cancer cells were stably transfected with an ERÎ±-specific short hairpin RNA that reduced endogenous ERÎ± . The resulting cell line was stably transfected with wild-type ERÎ± ( ER-AB cells ) , or ERÎ± containing serine to alanine mutation at S118 or S167 ( S118A cells and S167A cells , respectively ) . These stable cell lines expressed approximately equivalent ERÎ± compared with parental MCF-7 cells and were evaluated for growth , morphology , migration/invasion , and ERÎ±-regulated gene expression . S118A cells and S167A cells exhibited increased growth and migration/invasion in vitro . Forward- and side-scatter flow cytometry revealed that S167A cells were smaller in size , and both S118A and S167A cells exhibited less cellular complexity . S118A and S167A cells expressed pancytokeratin and membrane localization of Î²-catenin and did not express vimentin , indicating retention of epithelial lineage markers . Expression of ERÎ±-target genes and other genes regulated by ERÎ± signaling or involved in breast cancer were markedly altered in both S118A and S167A cells . In summary , attenuated phosphorylation of ERÎ± at S118 and S167 significantly affected cellular physiology and behavior in MCF-7 breast cancer cells , resulting in increased growth , migration/invasion , compromised expression of ERÎ± target genes , and markedly altered gene expression patterns .
    OUTPUT:
