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: Mutations in the tumor suppressor tuberin ( TSC2 ) are a common factor in the development of lymphangioleiomyomatosis ( LAM ) . LAM is a cystic lung disease that is characterized by the infiltration of smooth muscle-like cells into the pulmonary parenchyma . The mechanism by which the loss of tuberin promotes the development of LAM has yet to be elucidated , although several lines of evidence suggest it is due to the metastasis of tuberin-deficient cells . Here we show that tuberin-null cells become nonadherent and invasive . These nonadherent cells express cleaved forms of Î²-catenin . In reporter assays , the Î²-catenin products are transcriptionally active and promote MMP7 expression . Invasion by the tuberin-null cells is mediated by MMP7 . Examination of LAM tissues shows the expression of cleaved Î²-catenin products and MMP7 consistent with a model that tuberin-deficient cells acquire invasive properties through a Î²-catenin-dependent mechanism , which may underlie the development of LAM .
    OUTPUT:

agent
activating invasion and metastasis
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: Mutations in the tumor suppressor tuberin ( TSC2 ) are a common factor in the development of lymphangioleiomyomatosis ( LAM ) . LAM is a cystic lung disease that is characterized by the infiltration of smooth muscle-like cells into the pulmonary parenchyma . The mechanism by which the loss of tuberin promotes the development of LAM has yet to be elucidated , although several lines of evidence suggest it is due to the metastasis of tuberin-deficient cells . Here we show that tuberin-null cells become nonadherent and invasive . These nonadherent cells express cleaved forms of Î²-catenin . In reporter assays , the Î²-catenin products are transcriptionally active and promote MMP7 expression . Invasion by the tuberin-null cells is mediated by MMP7 . Examination of LAM tissues shows the expression of cleaved Î²-catenin products and MMP7 consistent with a model that tuberin-deficient cells acquire invasive properties through a Î²-catenin-dependent mechanism , which may underlie the development of LAM .
    OUTPUT:
