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 neurofibromatosis type 2 ( NF2 ) tumor suppressor gene encodes merlin , a membrane/cytoskeleton protein necessary for the maintenance of contact inhibition of growth in cells . Bi-allelic inactivation of NF2 is known to cause multiple cancers in both humans and mice . However , the mechanism through which merlin exerts its tumor-suppressive function remains obscure . In this report , we show that NF2 knockout mouse embryonic fibroblasts lost contact inhibition of cell proliferation and contained significantly increased canonical Wnt signaling . Inhibition of Rac1 , the activity of which is inversely regulated by NF2 , through the use of a dominant-negative mutant , small hairpin RNA or a small molecule inhibitor in NF2-deficient cells , was able to suppress elevated Wnt signals as shown by reduced activity of the T-cell factor 4 ( TCF4 ) transcription factor . Dominant-negative TCF4 or Rac1 mutant , as well as a small molecule inhibition of Wnt , were able to curb NF2 deficiency-elicited cell proliferation at the confluent state . Thus , Rac1-mediated canonical Wnt signaling is essential for the loss of contact inhibition in NF2-deficient cells .
    OUTPUT:

agent
evading growth suppressors
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 neurofibromatosis type 2 ( NF2 ) tumor suppressor gene encodes merlin , a membrane/cytoskeleton protein necessary for the maintenance of contact inhibition of growth in cells . Bi-allelic inactivation of NF2 is known to cause multiple cancers in both humans and mice . However , the mechanism through which merlin exerts its tumor-suppressive function remains obscure . In this report , we show that NF2 knockout mouse embryonic fibroblasts lost contact inhibition of cell proliferation and contained significantly increased canonical Wnt signaling . Inhibition of Rac1 , the activity of which is inversely regulated by NF2 , through the use of a dominant-negative mutant , small hairpin RNA or a small molecule inhibitor in NF2-deficient cells , was able to suppress elevated Wnt signals as shown by reduced activity of the T-cell factor 4 ( TCF4 ) transcription factor . Dominant-negative TCF4 or Rac1 mutant , as well as a small molecule inhibition of Wnt , were able to curb NF2 deficiency-elicited cell proliferation at the confluent state . Thus , Rac1-mediated canonical Wnt signaling is essential for the loss of contact inhibition in NF2-deficient cells .
    OUTPUT:
