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: The influence of radiation-induced apoptosis on radiosensitivity was studied in a set of closely related human lymphoblastoid cell lines differing in TP53 status . The clonogenic survival of irradiated TK6 cells ( expressing wild-type TP53 ) , WTK1 cells ( overexpressing mutant TP53 ) , and TK6E6 cells ( negative for TP53 owing to transfection with HPV16 E6 ) was assessed in relation to the induction of apoptosis and its suppression by caspase inhibition or treatment with PMA as well as after treatment with caffeine . Measurements using the alkaline comet assay and pulsed-field electrophoresis of the induction and repair of DNA strand breaks showed similar kinetics of the processing of early DNA damage in these cell lines . The cytochalasin B micronucleus assay revealed identical levels of residual damage in the first postirradiation mitosis of these cells . Abrogation of TP53-dependent apoptosis in TK6E6 cells resulted in a distinct increase in radioresistance . Further suppression of apoptosis as observed in WTK1 cells overexpressing mutant TP53 apparently was not responsible for the high radioresistance of WTK1 cells , since other means of highly efficient suppression of apoptosis ( caspase inhibition or PMA treatment ) increased the clonogenic survival of irradiated TK6 cells only to levels similar to those of TK6E6 cells with abrogated TP53-dependent apoptosis . Considering the similar levels of residual chromosomal damage in TK6E6 cells and WTK1 cells , a hitherto unknown mechanism of tolerance needs to be inferred for these TP53 mutant cells . This residual damage tolerance , however , appears to require an intact G2/M-phase checkpoint function since the relative radioresistance of the WTK1 cells was completely lost upon caffeine treatment , which also resulted in a failure of the TK6 and TK6E6 cells to execute apoptosis . In this situation , the cellular response seems to be dominated entirely by TP53-independent mitotic failure .
    OUTPUT:

agent
genomic instability and mutation;resisting cell death
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: The influence of radiation-induced apoptosis on radiosensitivity was studied in a set of closely related human lymphoblastoid cell lines differing in TP53 status . The clonogenic survival of irradiated TK6 cells ( expressing wild-type TP53 ) , WTK1 cells ( overexpressing mutant TP53 ) , and TK6E6 cells ( negative for TP53 owing to transfection with HPV16 E6 ) was assessed in relation to the induction of apoptosis and its suppression by caspase inhibition or treatment with PMA as well as after treatment with caffeine . Measurements using the alkaline comet assay and pulsed-field electrophoresis of the induction and repair of DNA strand breaks showed similar kinetics of the processing of early DNA damage in these cell lines . The cytochalasin B micronucleus assay revealed identical levels of residual damage in the first postirradiation mitosis of these cells . Abrogation of TP53-dependent apoptosis in TK6E6 cells resulted in a distinct increase in radioresistance . Further suppression of apoptosis as observed in WTK1 cells overexpressing mutant TP53 apparently was not responsible for the high radioresistance of WTK1 cells , since other means of highly efficient suppression of apoptosis ( caspase inhibition or PMA treatment ) increased the clonogenic survival of irradiated TK6 cells only to levels similar to those of TK6E6 cells with abrogated TP53-dependent apoptosis . Considering the similar levels of residual chromosomal damage in TK6E6 cells and WTK1 cells , a hitherto unknown mechanism of tolerance needs to be inferred for these TP53 mutant cells . This residual damage tolerance , however , appears to require an intact G2/M-phase checkpoint function since the relative radioresistance of the WTK1 cells was completely lost upon caffeine treatment , which also resulted in a failure of the TK6 and TK6E6 cells to execute apoptosis . In this situation , the cellular response seems to be dominated entirely by TP53-independent mitotic failure .
    OUTPUT:
