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: HGF signaling induces epithelial cells to disassemble cadherin-based adhesion and increase cell motility and invasion , a process termed epithelial-mesenchymal transition ( EMT ) . EMT plays a major role in cancer metastasis , allowing individual cells to detach from the primary tumor , invade local tissue , and colonize distant tissues with new tumors . While invasion of vascular and lymphatic networks is the predominant route of metastasis , nerves also can act as networks for dissemination of cancer cell to distant sites in a process termed perineual invasion ( PNI ) . Signaling between nerves and invasive cancer cells remains poorly understood , as does cellular decision making that selects the specific route of invasion . Here we examine how HGF signaling contributes to PNI using reductionist culture model systems . We find that TGFÎ² , produced by PC12 cells , enhances scattering in response to HGF stimulation , increasing both cell-cell junction disassembly and cell migration . Further , gradients of TGFÎ² induce migratory mesenchymal cells to undergo chemotaxis towards the source of TGFÎ² . Interestingly , VEGF suppresses TGFÎ²-induced enhancement of scattering . These results have broad implications for how combinatorial growth factor signaling contributes to cancer metastasis , suggesting that VEGF and TGFÎ² might modulate HGF signaling to influence route selection during cancer progression .
    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.
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    INPUT: HGF signaling induces epithelial cells to disassemble cadherin-based adhesion and increase cell motility and invasion , a process termed epithelial-mesenchymal transition ( EMT ) . EMT plays a major role in cancer metastasis , allowing individual cells to detach from the primary tumor , invade local tissue , and colonize distant tissues with new tumors . While invasion of vascular and lymphatic networks is the predominant route of metastasis , nerves also can act as networks for dissemination of cancer cell to distant sites in a process termed perineual invasion ( PNI ) . Signaling between nerves and invasive cancer cells remains poorly understood , as does cellular decision making that selects the specific route of invasion . Here we examine how HGF signaling contributes to PNI using reductionist culture model systems . We find that TGFÎ² , produced by PC12 cells , enhances scattering in response to HGF stimulation , increasing both cell-cell junction disassembly and cell migration . Further , gradients of TGFÎ² induce migratory mesenchymal cells to undergo chemotaxis towards the source of TGFÎ² . Interestingly , VEGF suppresses TGFÎ²-induced enhancement of scattering . These results have broad implications for how combinatorial growth factor signaling contributes to cancer metastasis , suggesting that VEGF and TGFÎ² might modulate HGF signaling to influence route selection during cancer progression .
    OUTPUT:
