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 Msh2 DNA mismatch repair gene is one of five genes implicated in the pathogenesis of hereditary nonpolyposis colorectal cancer ( HNPCC ) . To address the possible mechanisms of the site-specific occurrence of HNPCC , the effect of Msh2 deficiency on mutations in different parts of the colon was investigated using the BC-1(lacI)/Msh2 double transgenic mouse . Compared to the Msh2(+/+) mice , Msh2(-/-) mice had an 8-9-fold increase of mutation frequency ( MF ) in the lacI gene from the cecum and the proximal and distal colon . The mutational spectra were also significantly different between Msh2(+/+) and Msh2(-/-) mice , with a significant increase in the frequency of -1 frameshifts and G:C--&gt;A:T base substitutions in the repair-deficient mice . However , in spite of the site-specific predisposition of HNPCC in humans , we found no significant difference in the MF or mutation spectrum between the three parts of the colon in Msh2(+/+) , Msh2(+/-) , or Msh2(-/-) mice . In addition , 11 independent mutants harboring complex mutations within the lacI gene were recovered in the Msh2(-/-) mice . Interestingly , while the Msh2(+/-) mice displayed an overall MF similar to that observed in the wild-type mice , sequencing revealed a significantly different mutational spectrum between Msh2(+/+) and Msh2(+/-) mice , mainly characterized by an increase in -1 frameshifts . Due to the prevalence of frameshift mutations in HNPCC patients , this haploinsufficiency effect of the Msh2 gene in safeguarding genomic integrity may have important implications for human carrier status .
    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: The Msh2 DNA mismatch repair gene is one of five genes implicated in the pathogenesis of hereditary nonpolyposis colorectal cancer ( HNPCC ) . To address the possible mechanisms of the site-specific occurrence of HNPCC , the effect of Msh2 deficiency on mutations in different parts of the colon was investigated using the BC-1(lacI)/Msh2 double transgenic mouse . Compared to the Msh2(+/+) mice , Msh2(-/-) mice had an 8-9-fold increase of mutation frequency ( MF ) in the lacI gene from the cecum and the proximal and distal colon . The mutational spectra were also significantly different between Msh2(+/+) and Msh2(-/-) mice , with a significant increase in the frequency of -1 frameshifts and G:C--&gt;A:T base substitutions in the repair-deficient mice . However , in spite of the site-specific predisposition of HNPCC in humans , we found no significant difference in the MF or mutation spectrum between the three parts of the colon in Msh2(+/+) , Msh2(+/-) , or Msh2(-/-) mice . In addition , 11 independent mutants harboring complex mutations within the lacI gene were recovered in the Msh2(-/-) mice . Interestingly , while the Msh2(+/-) mice displayed an overall MF similar to that observed in the wild-type mice , sequencing revealed a significantly different mutational spectrum between Msh2(+/+) and Msh2(+/-) mice , mainly characterized by an increase in -1 frameshifts . Due to the prevalence of frameshift mutations in HNPCC patients , this haploinsufficiency effect of the Msh2 gene in safeguarding genomic integrity may have important implications for human carrier status .
    OUTPUT:
