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: Cellular senescence is the genetically programmed cessation of cellular proliferation . We have recently mapped a putative senescence gene(s) on the X chromosome of Chinese hamster embryo ( CHE ) cells . In the present study , we have utilized microcell-mediated chromosome transfer ( microcell fusion ) to test whether : ( i ) the human X chromosome exhibits similar genetic potential to induce senescence and ( ii ) the deletion or inactivation of the X-linked senescence gene(s) in CHE cells is associated with nickel-induced immortalization . A normal CHE or human X chromosome was first introduced into mouse-cell hybrids , then transferred by microcell fusion into a nickel-transformed , immortal male CHE cell line ( Ni-2/TGR ) with an X deletion ( Xq1 ) . Microcell fusion of the normal CHE X chromosome into tumorigenic Ni-2/TGR cells yielded senescence of all X recipient clones . The normal human X chromosome induced dominant senescence of tumorigenic Ni-2/TGR cells in only 17% of the resulting microcell hybrids ( 14/81 ) . Karyotypic analyses of 13 non-senescing human X chromosome-derived microcell hybrid clones revealed that none of these clones retained the complete X. A normal CHE X chromosome induced senescence of 75% of hybrids obtained with another immortal and tumorigenic nickel-transformed male CHE cell line ( Ni-6/TGR ) , which exhibited no visible deletion of the X chromosome , while the normal human X chromosome , only induced senescence in 19% of these hybrids . Transfer of the normal CHE or human X chromosome into spontaneously transformed and tumorigenic cell lines , CHO/TGR or V79/TGR , had little or no effect on their growth . These data suggest that both human and CHE cells possess similar X-linked genetic activities that regulate the process of cellular senescence , and that in Chinese hamster cells nickel-induced immortalization but not that of CHO or V79 cells is associated with inactivation of an X-linked senescence gene .
    OUTPUT:

agent
enabling replicative immortality
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: Cellular senescence is the genetically programmed cessation of cellular proliferation . We have recently mapped a putative senescence gene(s) on the X chromosome of Chinese hamster embryo ( CHE ) cells . In the present study , we have utilized microcell-mediated chromosome transfer ( microcell fusion ) to test whether : ( i ) the human X chromosome exhibits similar genetic potential to induce senescence and ( ii ) the deletion or inactivation of the X-linked senescence gene(s) in CHE cells is associated with nickel-induced immortalization . A normal CHE or human X chromosome was first introduced into mouse-cell hybrids , then transferred by microcell fusion into a nickel-transformed , immortal male CHE cell line ( Ni-2/TGR ) with an X deletion ( Xq1 ) . Microcell fusion of the normal CHE X chromosome into tumorigenic Ni-2/TGR cells yielded senescence of all X recipient clones . The normal human X chromosome induced dominant senescence of tumorigenic Ni-2/TGR cells in only 17% of the resulting microcell hybrids ( 14/81 ) . Karyotypic analyses of 13 non-senescing human X chromosome-derived microcell hybrid clones revealed that none of these clones retained the complete X. A normal CHE X chromosome induced senescence of 75% of hybrids obtained with another immortal and tumorigenic nickel-transformed male CHE cell line ( Ni-6/TGR ) , which exhibited no visible deletion of the X chromosome , while the normal human X chromosome , only induced senescence in 19% of these hybrids . Transfer of the normal CHE or human X chromosome into spontaneously transformed and tumorigenic cell lines , CHO/TGR or V79/TGR , had little or no effect on their growth . These data suggest that both human and CHE cells possess similar X-linked genetic activities that regulate the process of cellular senescence , and that in Chinese hamster cells nickel-induced immortalization but not that of CHO or V79 cells is associated with inactivation of an X-linked senescence gene .
    OUTPUT:
