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: DNA mismatch repair ( MMR ) is the process by which incorrectly paired DNA nucleotides are recognized and repaired . A germline mutation in one of the genes involved in the process may be responsible for a dominantly inherited cancer syndrome , hereditary nonpolyposis colon cancer . Cancer progression in predisposed individuals results from the somatic inactivation of the normal copy of the MMR gene , leading to a mutator phenotype affecting preferentially repeat sequences ( microsatellite instability , MSI ) . Recently , we identified children with a constitutional deficiency of MMR activity attributable to a mutation in the h MLH1 gene . These children exhibited a constitutional genetic instability associated with clinical features of de novo neurofibromatosis type 1 ( NF1 ) and early onset of extracolonic cancer . Based on these observations , we hypothesized that somatic NF1 gene mutation was a frequent and possibly early event in MMR-deficient cells . To test this hypothesis , we screened for NF1 mutations in cancer cells . Genetic alterations were identified in five out of ten tumor cell lines with MSI , whereas five MMR-proficient tumor cell lines expressed a wild-type NF1 gene . Somatic NF1 mutations were also detected in two primary tumors exhibiting an MSI phenotype . Finally , a 35-bp deletion in the murine Nf1 coding region was identified in mlh1-/- mouse embryonic fibroblasts . These observations demonstrate that the NF1 gene is a mutational target of MMR deficiency and suggest that its inactivation is an important step of the malignant progression of MMR-deficient cells .
    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.
    ###
    INPUT: DNA mismatch repair ( MMR ) is the process by which incorrectly paired DNA nucleotides are recognized and repaired . A germline mutation in one of the genes involved in the process may be responsible for a dominantly inherited cancer syndrome , hereditary nonpolyposis colon cancer . Cancer progression in predisposed individuals results from the somatic inactivation of the normal copy of the MMR gene , leading to a mutator phenotype affecting preferentially repeat sequences ( microsatellite instability , MSI ) . Recently , we identified children with a constitutional deficiency of MMR activity attributable to a mutation in the h MLH1 gene . These children exhibited a constitutional genetic instability associated with clinical features of de novo neurofibromatosis type 1 ( NF1 ) and early onset of extracolonic cancer . Based on these observations , we hypothesized that somatic NF1 gene mutation was a frequent and possibly early event in MMR-deficient cells . To test this hypothesis , we screened for NF1 mutations in cancer cells . Genetic alterations were identified in five out of ten tumor cell lines with MSI , whereas five MMR-proficient tumor cell lines expressed a wild-type NF1 gene . Somatic NF1 mutations were also detected in two primary tumors exhibiting an MSI phenotype . Finally , a 35-bp deletion in the murine Nf1 coding region was identified in mlh1-/- mouse embryonic fibroblasts . These observations demonstrate that the NF1 gene is a mutational target of MMR deficiency and suggest that its inactivation is an important step of the malignant progression of MMR-deficient cells .
    OUTPUT:
