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: PURPOSE Genomic complexity is present in approximately 15% to 30% of all chronic lymphocytic leukemia ( CLL ) and has emerged as a strong independent predictor of rapid disease progression and short remission duration in CLL . We conducted this study to advance our understanding of the causes of genomic complexity in CLL . EXPERIMENTAL DESIGN We have obtained quantitative measurements of radiation-induced apoptosis and radiation-induced ATM autophosphorylation in purified CLL cells from 158 and 140 patients , respectively , and have used multivariate analysis to identify independent contributions of various biological variables on genomic complexity in CLL . RESULTS Here , we identify a strong independent effect of radiation resistance on elevated genomic complexity in CLL and describe radiation resistance as a predictor for shortened CLL survival . Furthermore , using multivariate analysis , we identify del17p/p53 aberrations , del11q , del13q14 type II ( invariably resulting in Rb loss ) , and CD38 expression as independent predictors of genomic complexity in CLL , with aberrant p53 as a predictor of approximately 50% of genomic complexity in CLL . Focusing on del11q , we determined that normalized ATM activity was a modest predictor of genomic complexity but was not independent of del11q . Through single nucleotide polymorphism array-based fine mapping of del11q , we identified frequent monoallelic loss of Mre11 and H2AFX in addition to ATM , indicative of compound del11q-resident gene defects in the DNA double-strand break response . CONCLUSIONS Our quantitative analysis links multiple molecular defects , including for the first time del11q and large 13q14 deletions ( type II ) , to elevated genomic complexity in CLL , thereby suggesting mechanisms for the observed clinical aggressiveness of CLL in patients with unstable genomes .
    OUTPUT:

agent
genomic instability and mutation
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: PURPOSE Genomic complexity is present in approximately 15% to 30% of all chronic lymphocytic leukemia ( CLL ) and has emerged as a strong independent predictor of rapid disease progression and short remission duration in CLL . We conducted this study to advance our understanding of the causes of genomic complexity in CLL . EXPERIMENTAL DESIGN We have obtained quantitative measurements of radiation-induced apoptosis and radiation-induced ATM autophosphorylation in purified CLL cells from 158 and 140 patients , respectively , and have used multivariate analysis to identify independent contributions of various biological variables on genomic complexity in CLL . RESULTS Here , we identify a strong independent effect of radiation resistance on elevated genomic complexity in CLL and describe radiation resistance as a predictor for shortened CLL survival . Furthermore , using multivariate analysis , we identify del17p/p53 aberrations , del11q , del13q14 type II ( invariably resulting in Rb loss ) , and CD38 expression as independent predictors of genomic complexity in CLL , with aberrant p53 as a predictor of approximately 50% of genomic complexity in CLL . Focusing on del11q , we determined that normalized ATM activity was a modest predictor of genomic complexity but was not independent of del11q . Through single nucleotide polymorphism array-based fine mapping of del11q , we identified frequent monoallelic loss of Mre11 and H2AFX in addition to ATM , indicative of compound del11q-resident gene defects in the DNA double-strand break response . CONCLUSIONS Our quantitative analysis links multiple molecular defects , including for the first time del11q and large 13q14 deletions ( type II ) , to elevated genomic complexity in CLL , thereby suggesting mechanisms for the observed clinical aggressiveness of CLL in patients with unstable genomes .
    OUTPUT:
