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.
    ###
    INPUT: To characterize the impact of increased production of TGF-beta in a xenograft model of human breast cancer , TGF-beta-responsive MDA-231 cells were genetically modified by stable transfection so as to increase their production of active TGF-beta1 . Compared with control cells , cells that produced increased amounts of TGF-beta proliferated in vitro more slowly . In vivo , however , tumors derived from these cells exhibited increased proliferation and grew at an accelerated pace . To evaluate the role of autocrine TGF-beta signaling , cells were also transfected with a dominant-negative truncated type II TGF-beta receptor ( TbetaRII ) . Disruption of autocrine TGF-beta signaling in the TGF-beta-overexpressing cells reduced their in vivo growth rate . Co-inoculation of Matrigel with the TGF-beta-overexpressing cells expressing the truncated TbetaRII compensated for their diminished in vivo growth capacity , compared with the TGF-beta-overexpressing cells with an intact autocrine loop . Tissue invasion by the tumor was a distinctive feature of the TGF-beta-overexpressing cells , whether or not the autocrine loop was intact . Furthermore , tumors derived from TGF-beta-overexpressing cells , irrespective of the status of the autocrine TGF-beta-signaling pathway , had a higher incidence of lung metastasis . Consistent with the suggestion that TGF-beta's enhancement of invasion and metastasis is paracrine-based , we observed no significant differences among the cell clones in an in vitro invasion assay . Thus , in this experimental model system in vitro assays of cell proliferation and invasion do not accurately reflect in vivo observations , perhaps due to autocrine and paracrine effects of TGF-beta that influence the important in vivo-based phenomena of tumor growth , invasion , and metastasis .
    OUTPUT:

agent
sustaining proliferative signaling;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.
    ###
    INPUT: To characterize the impact of increased production of TGF-beta in a xenograft model of human breast cancer , TGF-beta-responsive MDA-231 cells were genetically modified by stable transfection so as to increase their production of active TGF-beta1 . Compared with control cells , cells that produced increased amounts of TGF-beta proliferated in vitro more slowly . In vivo , however , tumors derived from these cells exhibited increased proliferation and grew at an accelerated pace . To evaluate the role of autocrine TGF-beta signaling , cells were also transfected with a dominant-negative truncated type II TGF-beta receptor ( TbetaRII ) . Disruption of autocrine TGF-beta signaling in the TGF-beta-overexpressing cells reduced their in vivo growth rate . Co-inoculation of Matrigel with the TGF-beta-overexpressing cells expressing the truncated TbetaRII compensated for their diminished in vivo growth capacity , compared with the TGF-beta-overexpressing cells with an intact autocrine loop . Tissue invasion by the tumor was a distinctive feature of the TGF-beta-overexpressing cells , whether or not the autocrine loop was intact . Furthermore , tumors derived from TGF-beta-overexpressing cells , irrespective of the status of the autocrine TGF-beta-signaling pathway , had a higher incidence of lung metastasis . Consistent with the suggestion that TGF-beta's enhancement of invasion and metastasis is paracrine-based , we observed no significant differences among the cell clones in an in vitro invasion assay . Thus , in this experimental model system in vitro assays of cell proliferation and invasion do not accurately reflect in vivo observations , perhaps due to autocrine and paracrine effects of TGF-beta that influence the important in vivo-based phenomena of tumor growth , invasion , and metastasis .
    OUTPUT:
