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: Neurofibromatosis type 2 patients develop schwannomas , meningiomas and ependymomas resulting from mutations in the tumor suppressor gene , NF2 , encoding a membrane-cytoskeleton adapter protein called merlin . Merlin regulates contact inhibition of growth and controls the availability of growth factor receptors at the cell surface . We tested if microtubule-based vesicular trafficking might be a mechanism by which merlin acts . We found that schwannoma cells , containing merlin mutations and constitutive activation of the Rho/Rac family of GTPases , had decreased intracellular vesicular trafficking relative to normal human Schwann cells . In Nf2-/- mouse Schwann ( SC4 ) cells , re-expression of merlin as well as inhibition of Rac or its effector kinases , MLK and p38(SAPK) , each increased the velocity of Rab6 positive exocytic vesicles . Conversely , an activated Rac mutant decreased Rab6 vesicle velocity . Vesicle motility assays in isolated squid axoplasm further demonstrated that both mutant merlin and active Rac specifically reduce anterograde microtubule-based transport of vesicles dependent upon the activity of p38(SAPK) kinase . Taken together , our data suggest loss of merlin results in the Rac-dependent decrease of anterograde trafficking of exocytic vesicles , representing a possible mechanism controlling the concentration of growth factor receptors at the cell surface .
    OUTPUT:

agent
genomic instability and mutation;sustaining proliferative signaling
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: Neurofibromatosis type 2 patients develop schwannomas , meningiomas and ependymomas resulting from mutations in the tumor suppressor gene , NF2 , encoding a membrane-cytoskeleton adapter protein called merlin . Merlin regulates contact inhibition of growth and controls the availability of growth factor receptors at the cell surface . We tested if microtubule-based vesicular trafficking might be a mechanism by which merlin acts . We found that schwannoma cells , containing merlin mutations and constitutive activation of the Rho/Rac family of GTPases , had decreased intracellular vesicular trafficking relative to normal human Schwann cells . In Nf2-/- mouse Schwann ( SC4 ) cells , re-expression of merlin as well as inhibition of Rac or its effector kinases , MLK and p38(SAPK) , each increased the velocity of Rab6 positive exocytic vesicles . Conversely , an activated Rac mutant decreased Rab6 vesicle velocity . Vesicle motility assays in isolated squid axoplasm further demonstrated that both mutant merlin and active Rac specifically reduce anterograde microtubule-based transport of vesicles dependent upon the activity of p38(SAPK) kinase . Taken together , our data suggest loss of merlin results in the Rac-dependent decrease of anterograde trafficking of exocytic vesicles , representing a possible mechanism controlling the concentration of growth factor receptors at the cell surface .
    OUTPUT:
