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: Oncogene-induced senescence can provide a protective mechanism against tumour progression . However , production of cytokines and growth factors by senescent cells may contribute to tumour development . Thus , it is unclear whether induction of senescence represents a viable therapeutic approach . Here , using a mouse model with orthotopic implantation of metastatic melanoma tumours taken from 19 patients , we observed that targeting aurora kinases with MLN8054/MLN8237 impaired mitosis , induced senescence and markedly blocked proliferation in patient tumour implants . Importantly , when a subset of tumour-bearing mice were monitored for tumour progression after pausing MLN8054 treatment , 50% of the tumours did not progress over a 12-month period . Mechanistic analyses revealed that inhibition of aurora kinases induced polyploidy and the ATM/Chk2 DNA damage response , which mediated senescence and a NF-ÎºB-related , senescence-associated secretory phenotype ( SASP ) . Blockade of IKKÎ²/NF-ÎºB led to reversal of MLN8237-induced senescence and SASP . Results demonstrate that removal of senescent tumour cells by infiltrating myeloid cells is crucial for inhibition of tumour re-growth . Altogether , these data demonstrate that induction of senescence , coupled with immune surveillance , can limit melanoma growth .
    OUTPUT:

agent
enabling replicative immortality;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.
    ###
    INPUT: Oncogene-induced senescence can provide a protective mechanism against tumour progression . However , production of cytokines and growth factors by senescent cells may contribute to tumour development . Thus , it is unclear whether induction of senescence represents a viable therapeutic approach . Here , using a mouse model with orthotopic implantation of metastatic melanoma tumours taken from 19 patients , we observed that targeting aurora kinases with MLN8054/MLN8237 impaired mitosis , induced senescence and markedly blocked proliferation in patient tumour implants . Importantly , when a subset of tumour-bearing mice were monitored for tumour progression after pausing MLN8054 treatment , 50% of the tumours did not progress over a 12-month period . Mechanistic analyses revealed that inhibition of aurora kinases induced polyploidy and the ATM/Chk2 DNA damage response , which mediated senescence and a NF-ÎºB-related , senescence-associated secretory phenotype ( SASP ) . Blockade of IKKÎ²/NF-ÎºB led to reversal of MLN8237-induced senescence and SASP . Results demonstrate that removal of senescent tumour cells by infiltrating myeloid cells is crucial for inhibition of tumour re-growth . Altogether , these data demonstrate that induction of senescence , coupled with immune surveillance , can limit melanoma growth .
    OUTPUT:
