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: Several members of the phosphatidylinositol 3-kinase family play key roles in recognising and responding to damage in DNA , induced by a variety of chemicals and other agents . One of these , ATM , the product of the gene mutated in the human genetic disorder ataxia-telangiectasia ( A-T ) , recognises double strand breaks in DNA caused by ionizing radiation and radiomimetic chemicals . In order to study DNA damage recognition and the abnormalities of genome instability and cancer predisposition that occur in A-T patients , we generated a mouse model expressing a mutant form of Atm corresponding to a common human mutation . In this model , a 9 nucleotide in-frame deletion was introduced into the Atm gene and has been designated Atm-Delta SRI . These animals had a longer lifespan than Atm gene disrupted mice ( Atm(-/-) ) and they developed less thymic lymphomas . A characteristic of the lymphomas appearing in Atm-Delta SRI mice was an increased rate of apoptosis compared to the corresponding tumours in Atm(-/-) mice . Increased expression of FasL in these tumours may account for the higher levels of apoptosis . These results demonstrate that expression of mutant Atm in mice gives rise to phenotypic differences compared to Atm(-/-) mice and has implications for heterogeneity described in the human syndrome .
    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.
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    INPUT: Several members of the phosphatidylinositol 3-kinase family play key roles in recognising and responding to damage in DNA , induced by a variety of chemicals and other agents . One of these , ATM , the product of the gene mutated in the human genetic disorder ataxia-telangiectasia ( A-T ) , recognises double strand breaks in DNA caused by ionizing radiation and radiomimetic chemicals . In order to study DNA damage recognition and the abnormalities of genome instability and cancer predisposition that occur in A-T patients , we generated a mouse model expressing a mutant form of Atm corresponding to a common human mutation . In this model , a 9 nucleotide in-frame deletion was introduced into the Atm gene and has been designated Atm-Delta SRI . These animals had a longer lifespan than Atm gene disrupted mice ( Atm(-/-) ) and they developed less thymic lymphomas . A characteristic of the lymphomas appearing in Atm-Delta SRI mice was an increased rate of apoptosis compared to the corresponding tumours in Atm(-/-) mice . Increased expression of FasL in these tumours may account for the higher levels of apoptosis . These results demonstrate that expression of mutant Atm in mice gives rise to phenotypic differences compared to Atm(-/-) mice and has implications for heterogeneity described in the human syndrome .
    OUTPUT:
